General Information of the m6A Target Gene (ID: M6ATAR00339)
Target Name Serine/threonine-protein kinase mTOR (MTOR)
Synonyms
FK506-binding protein 12-rapamycin complex-associated protein 1; FKBP12-rapamycin complex-associated protein; Mammalian target of rapamycin; mTOR; Mechanistic target of rapamycin; Rapamycin and FKBP12 target 1; Rapamycin target protein 1; FRAP; FRAP1; FRAP2; RAFT1; RAPT1
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Gene Name MTOR
Chromosomal Location 1p36.22
Family PI3/PI4-kinase family
Function
Serine/threonine protein kinase which is a central regulator of cellular metabolism, growth and survival in response to hormones, growth factors, nutrients, energy and stress signals. MTOR directly or indirectly regulates the phosphorylation of at least 800 proteins. Functions as part of 2 structurally and functionally distinct signaling complexes mTORC1 and mTORC2 (mTOR complex 1 and 2). Activated mTORC1 up-regulates protein synthesis by phosphorylating key regulators of mRNA translation and ribosome synthesis. This includes phosphorylation of EIF4EBP1 and release of its inhibition toward the elongation initiation factor 4E (eiF4E) (By similarity). Moreover, phosphorylates and activates RPS6KB1 and RPS6KB2 that promote protein synthesis by modulating the activity of their downstream targets including ribosomal protein S6, eukaryotic translation initiation factor EIF4B, and the inhibitor of translation initiation PDCD4. This also includes mTORC1 signaling cascade controlling the MiT/TFE factors TFEB and TFE3: in the presence of nutrients, mediates phosphorylation of TFEB and TFE3, promoting their cytosolic retention and inactivation. Upon starvation or lysosomal stress, inhibition of mTORC1 induces dephosphorylation and nuclear translocation of TFEB and TFE3, promoting their transcription factor activity. Stimulates the pyrimidine biosynthesis pathway, both by acute regulation through RPS6KB1-mediated phosphorylation of the biosynthetic enzyme CAD, and delayed regulation, through transcriptional enhancement of the pentose phosphate pathway which produces 5-phosphoribosyl-1-pyrophosphate (PRPP), an allosteric activator of CAD at a later step in synthesis, this function is dependent on the mTORC1 complex . Regulates ribosome synthesis by activating RNA polymerase III-dependent transcription through phosphorylation and inhibition of MAF1 an RNA polymerase III-repressor . In parallel to protein synthesis, also regulates lipid synthesis through SREBF1/SREBP1 and LPIN1 (By similarity). To maintain energy homeostasis mTORC1 may also regulate mitochondrial biogenesis through regulation of PPARGC1A (By similarity). mTORC1 also negatively regulates autophagy through phosphorylation of ULK1 (By similarity). Under nutrient sufficiency, phosphorylates ULK1 at 'Ser-758', disrupting the interaction with AMPK and preventing activation of ULK1 (By similarity). Also prevents autophagy through phosphorylation of the autophagy inhibitor DAP. Also prevents autophagy by phosphorylating RUBCNL/Pacer under nutrient-rich conditions. Prevents autophagy by mediating phosphorylation of AMBRA1, thereby inhibiting AMBRA1 ability to mediate ubiquitination of ULK1 and interaction between AMBRA1 and PPP2CA . mTORC1 exerts a feedback control on upstream growth factor signaling that includes phosphorylation and activation of GRB10 a INSR-dependent signaling suppressor. Among other potential targets mTORC1 may phosphorylate CLIP1 and regulate microtubules. As part of the mTORC2 complex MTOR may regulate other cellular processes including survival and organization of the cytoskeleton. Plays a critical role in the phosphorylation at 'Ser-473' of AKT1, a pro-survival effector of phosphoinositide 3-kinase, facilitating its activation by PDK1. mTORC2 may regulate the actin cytoskeleton, through phosphorylation of PRKCA, PXN and activation of the Rho-type guanine nucleotide exchange factors RHOA and RAC1A or RAC1B. mTORC2 also regulates the phosphorylation of SGK1 at 'Ser-422'. Regulates osteoclastogenesis by adjusting the expression of CEBPB isoforms (By similarity). Plays an important regulatory role in the circadian clock function; regulates period length and rhythm amplitude of the suprachiasmatic nucleus (SCN) and liver clocks (By similarity). Phosphorylates SQSTM1, promoting interaction between SQSTM1 and KEAP1 and subsequent inactivation of the BCR(KEAP1) complex (By similarity).
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Gene ID 2475
Uniprot ID
MTOR_HUMAN
HGNC ID
HGNC:3942
Ensembl Gene ID
ENSG00000198793
KEGG ID
hsa:2475
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
MTOR can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
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Methyltransferase-like 3 (METTL3) [WRITER]
Representative RNA-seq result indicating the expression of this target gene regulated by METTL3
Cell Line Liver Mus musculus
Treatment: Mettl3 knockout liver
Control: Wild type liver cells
GSE198512
Regulation
logFC: 8.34E-01
p-value: 1.58E-02
More Results Click to View More RNA-seq Results
Representative RIP-seq result supporting the interaction between MTOR and the regulator
Cell Line MDA-MB-231 Homo sapiens
Regulation logFC: 1.47E+00 GSE60213
In total 4 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary METTL3-mediated m6 A methylation promotes lung cancer progression via activating PI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) pathway.
Target Regulation Up regulation
Responsed Disease Lung cancer ICD-11: 2C25
Pathway Response mTOR signaling pathway hsa04150
PI3K-Akt signaling pathway hsa04151
In-vitro Model A-549 Lung adenocarcinoma Homo sapiens CVCL_0023
In-vivo Model 5 × 106 A549 cells overexpressing METTL3 (Lv-METTL3) or control (Lv-Ctrl) were suspended in 100?uL phosphate-buffered saline (PBS), and were subcutaneously injected into mouse lower right flank. Drug treatment started in the Lv-METTL3 group when the tumour volume reached around 100 mm3. Mice were randomly divided into three groups to receive vehicle, GSK2536771 (30 mg/kg) or rapamycin (1 mg/kg). Drugs were administrated daily through intraperitoneal injection for 18 days. Treatment conditions were chosen as previously reported.
Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene [2]
Response Summary Knockdown of METTL3 could obviously promote cell proliferation, migration and invasion function, and induce G0/G1 arrest,METTL3 acts as a novel marker for tumorigenesis, development and survival of RCC. Knockdown of METTL3 promoted changes in pI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) markers' expression with a gain in p-PI3k, p-AKT, p-mTOR and p-p70, and a loss of p-4EBP1.
Target Regulation Down regulation
Responsed Disease Renal cell carcinoma ICD-11: 2C90
Cell Process Epithelial-to-mesenchymal transition
Arrest cell cycle at G0/G1 phase
In-vitro Model ACHN Papillary renal cell carcinoma Homo sapiens CVCL_1067
Caki-1 Clear cell renal cell carcinoma Homo sapiens CVCL_0234
Caki-2 Papillary renal cell carcinoma Homo sapiens CVCL_0235
HK2 Normal Acipenser baerii CVCL_YE28
In-vivo Model Cells (5×106 cells in 200 uL) were suspended with 100 uL PBS and 100 uL Matrigel Matrix, and injected subcutaneously into the left armpit of each mouse.
Experiment 3 Reporting the m6A Methylation Regulator of This Target Gene [3]
Response Summary METTL3 promotes the progression of retinoblastoma through PI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) pathways in vitro and in vivo. METTL3 has an impact on the PI3K-AKT-mTOR-P70S6K/4EBP1 pathway. The cell proliferation results show that the stimulatory function of METTL3 is lost after rapamycin treatment.
Target Regulation Up regulation
Responsed Disease Retinoblastoma ICD-11: 2D02.2
Pathway Response PI3K-Akt signaling pathway hsa04151
mTOR signaling pathway hsa04150
Cell Process Cell proliferation
Cell migration
Cell invasion
Cell apoptosis
In-vitro Model WERI-Rb-1 Retinoblastoma Homo sapiens CVCL_1792
Y-79 Retinoblastoma Homo sapiens CVCL_1893
In-vivo Model To establish a subcutaneous tumour model in nude mice, 2 × 107 Y79 cells (METTL3 knockdown group: shNC, shRNA1 and shRNA2; METTL3 up-regulated group: NC and METLL3) were resuspended in 1 mL of pre-cooled PBS, and 200 uL of the cell suspension was injected subcutaneously into the left side of the armpit to investigate tumour growth (4 × 106 per mouse).
Experiment 4 Reporting the m6A Methylation Regulator of This Target Gene [4]
Response Summary The contribution of METTL3-mediated m6A modification of Ddit4 mRNA to macrophage metabolic reprogramming in non-alcoholic fatty liver disease and obesity. In METTL3-deficient macrophages, there is a significant downregulation of Serine/threonine-protein kinase mTOR (MTOR) and nuclear factor Kappa-B (NF-Kappa-B) pathway activity in response to cellular stress and cytokine stimulation, which can be restored by knockdown of DDIT4.
Target Regulation Up regulation
Responsed Disease Non-alcoholic fatty liver disease ICD-11: DB92
Pathway Response mTOR signaling pathway hsa04150
HIF-1 signaling pathway hsa04066
In-vivo Model The 8-10 weeks old mice were fed either a high fat diet or HF-CDAA , ad lib for 6-12 weeks. Chow diet was used as control for HFD.The mouse liver was perfused with PBS through portal vein, and liver tissue was cut into small pieces by a scissor. The single cell was made using syringe plunger to mull the tissue, and passed through a 40 uM cell strainer.
YTH domain-containing family protein 1 (YTHDF1) [READER]
Representative RIP-seq result supporting the interaction between MTOR and the regulator
Cell Line Hela Homo sapiens
Regulation logFC: 1.73E+00 GSE63591
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [5]
Response Summary YTHDF1 contributes to the progression of HCC by activating PI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) signaling pathway and inducing EMT.
Target Regulation Down regulation
Responsed Disease Hepatocellular carcinoma ICD-11: 2C12.02
Pathway Response PI3K-Akt signaling pathway hsa04151), mTOR signaling pathway
Cell Process Epithelial-mesenchymal transition
Cell migration
Cell invasion
Cell proliferation
In-vitro Model SNU-398 Adult hepatocellular carcinoma Homo sapiens CVCL_0077
SK-HEP-1 Liver and intrahepatic bile duct epithelial neoplasm Homo sapiens CVCL_0525
PLC/PRF/5 Adult hepatocellular carcinoma Homo sapiens CVCL_0485
L-02 Endocervical adenocarcinoma Homo sapiens CVCL_6926
Huh-7 Adult hepatocellular carcinoma Homo sapiens CVCL_0336
Hep-G2 Hepatoblastoma Homo sapiens CVCL_0027
Hep 3B2.1-7 Childhood hepatocellular carcinoma Homo sapiens CVCL_0326
HEK293T Normal Homo sapiens CVCL_0063
HCCLM3 Adult hepatocellular carcinoma Homo sapiens CVCL_6832
In-vivo Model Ten four-week-old BALB/c male nude mice (GemPharmatech, Jiangsu, China) were subcutaneously injected with control Huh7 cells 2 × 106 (left-back) and stable knockdown of YTHDF1 Huh7 cells 2 × 106 (right-back). These cells were respectively premixed with 50 ul Matrigel (Corning, 354,234) in 100 ul PBS.
Fat mass and obesity-associated protein (FTO) [ERASER]
In total 4 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition.
Responsed Disease Colorectal cancer ICD-11: 2B91
Responsed Drug Asparagine inhibitor Approved
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition.
Responsed Disease Colorectal cancer ICD-11: 2B91
Responsed Drug Chloroquine Approved
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 3 Reporting the m6A Methylation Regulator of This Target Gene [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition.
Responsed Disease Colorectal cancer ICD-11: 2B91
Responsed Drug Meclofenamate sodium Approved
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 4 Reporting the m6A Methylation Regulator of This Target Gene [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition.
Responsed Disease Colorectal cancer ICD-11: 2B91
Responsed Drug CB-839 Phase 2
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Methyltransferase-like 14 (METTL14) [WRITER]
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [7]
Response Summary The m6A modification level was decreased in GC and METTL14 was a key regulator resulting in m6A disorder in GC. METTL14 overexpression suppressed GC cell proliferation and aggression by deactivating the PI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) pathway and the EMT pathway, respectively.
Target Regulation Down regulation
Responsed Disease Gastric cancer ICD-11: 2B72
Pathway Response PI3K-Akt signaling pathway hsa04151
mTOR signaling pathway hsa04150
In-vitro Model SGC-7901 Gastric carcinoma Homo sapiens CVCL_0520
MGC-803 Gastric mucinous adenocarcinoma Homo sapiens CVCL_5334
GES-1 Normal Homo sapiens CVCL_EQ22
YTH domain-containing family protein 2 (YTHDF2) [READER]
In total 4 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulation Up regulation
Responsed Disease Colorectal cancer ICD-11: 2B91
Responsed Drug Asparagine inhibitor Approved
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulation Up regulation
Responsed Disease Colorectal cancer ICD-11: 2B91
Responsed Drug Chloroquine Approved
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 3 Reporting the m6A Methylation Regulator of This Target Gene [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulation Up regulation
Responsed Disease Colorectal cancer ICD-11: 2B91
Responsed Drug Meclofenamate sodium Approved
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 4 Reporting the m6A Methylation Regulator of This Target Gene [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulation Up regulation
Responsed Disease Colorectal cancer ICD-11: 2B91
Responsed Drug CB-839 Phase 2
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Gastric cancer [ICD-11: 2B72]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [7]
Response Summary The m6A modification level was decreased in GC and METTL14 was a key regulator resulting in m6A disorder in GC. METTL14 overexpression suppressed GC cell proliferation and aggression by deactivating the PI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) pathway and the EMT pathway, respectively.
Responsed Disease Gastric cancer [ICD-11: 2B72]
Target Regulator Methyltransferase-like 14 (METTL14) WRITER
Target Regulation Down regulation
Pathway Response PI3K-Akt signaling pathway hsa04151
mTOR signaling pathway hsa04150
In-vitro Model SGC-7901 Gastric carcinoma Homo sapiens CVCL_0520
MGC-803 Gastric mucinous adenocarcinoma Homo sapiens CVCL_5334
GES-1 Normal Homo sapiens CVCL_EQ22
Colorectal cancer [ICD-11: 2B91]
In total 5 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response []
Response Summary WM_Score correlated highly with the regulation of transcription and post-transcriptional events contributing to the development of colorectal cancer. In response to anti-cancer drugs, WM_Score highly negatively correlated (drug sensitive) with drugs which targeted oncogenic related pathways, such as MAPK, EGFR, and Serine/threonine-protein kinase mTOR (MTOR) signaling pathways, positively correlated (drug resistance) with drugs which targeted in apoptosis and cell cycle. Importantly, the WM_Score was associated with the therapeutic efficacy of PD-L1 blockade, suggesting that the development of potential drugs targeting these "writers" to aid the clinical benefits of immunotherapy.
Responsed Disease Colorectal cancer [ICD-11: 2B91]
Pathway Response MAPK signaling pathway hsa04010
VEGF signaling pathway hsa04370
mTOR signaling pathway hsa04150
PD-L1 expression and PD-1 checkpoint pathway in cancer hsa05235
Cell Process Cell apoptosis
Experiment 2 Reporting the m6A-centered Disease Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition.
Responsed Disease Colorectal cancer [ICD-11: 2B91]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Responsed Drug Asparagine inhibitor Approved
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 3 Reporting the m6A-centered Disease Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition.
Responsed Disease Colorectal cancer [ICD-11: 2B91]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Responsed Drug Chloroquine Approved
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 4 Reporting the m6A-centered Disease Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition.
Responsed Disease Colorectal cancer [ICD-11: 2B91]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Responsed Drug Meclofenamate sodium Approved
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 5 Reporting the m6A-centered Disease Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition.
Responsed Disease Colorectal cancer [ICD-11: 2B91]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Responsed Drug CB-839 Phase 2
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Gastrointestinal cancer [ICD-11: 2C11]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response []
Response Summary m6A regulators were mostly upregulated in Gastrointestinal cancer and their differential expression significantly influenced the overall survival of patients with GI cancer. The phosphatidylinositol-3-kinase (PI3K)/Akt and mammalian target of rapamycin Serine/threonine-protein kinase mTOR (MTOR) signaling pathways were found to be potentially affected by m6A modification in most human cancers, including GI cancer, which was further verified by m6A-Seq and phospho-MAPK array.
Responsed Disease Gastrointestinal cancer [ICD-11: 2C11]
Pathway Response PI3K-Akt signaling pathway hsa04151), mTOR signaling pathway
In-vitro Model ()
()
Huh-7 Adult hepatocellular carcinoma Homo sapiens CVCL_0336
HCT 116 Colon carcinoma Homo sapiens CVCL_0291
Liver cancer [ICD-11: 2C12]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [5]
Response Summary YTHDF1 contributes to the progression of HCC by activating PI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) signaling pathway and inducing EMT.
Responsed Disease Hepatocellular carcinoma [ICD-11: 2C12.02]
Target Regulator YTH domain-containing family protein 1 (YTHDF1) READER
Target Regulation Down regulation
Pathway Response PI3K-Akt signaling pathway hsa04151), mTOR signaling pathway
Cell Process Epithelial-mesenchymal transition
Cell migration
Cell invasion
Cell proliferation
In-vitro Model SNU-398 Adult hepatocellular carcinoma Homo sapiens CVCL_0077
SK-HEP-1 Liver and intrahepatic bile duct epithelial neoplasm Homo sapiens CVCL_0525
PLC/PRF/5 Adult hepatocellular carcinoma Homo sapiens CVCL_0485
L-02 Endocervical adenocarcinoma Homo sapiens CVCL_6926
Huh-7 Adult hepatocellular carcinoma Homo sapiens CVCL_0336
Hep-G2 Hepatoblastoma Homo sapiens CVCL_0027
Hep 3B2.1-7 Childhood hepatocellular carcinoma Homo sapiens CVCL_0326
HEK293T Normal Homo sapiens CVCL_0063
HCCLM3 Adult hepatocellular carcinoma Homo sapiens CVCL_6832
In-vivo Model Ten four-week-old BALB/c male nude mice (GemPharmatech, Jiangsu, China) were subcutaneously injected with control Huh7 cells 2 × 106 (left-back) and stable knockdown of YTHDF1 Huh7 cells 2 × 106 (right-back). These cells were respectively premixed with 50 ul Matrigel (Corning, 354,234) in 100 ul PBS.
Lung cancer [ICD-11: 2C25]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary METTL3-mediated m6 A methylation promotes lung cancer progression via activating PI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) pathway.
Responsed Disease Lung cancer [ICD-11: 2C25]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Pathway Response mTOR signaling pathway hsa04150
PI3K-Akt signaling pathway hsa04151
In-vitro Model A-549 Lung adenocarcinoma Homo sapiens CVCL_0023
In-vivo Model 5 × 106 A549 cells overexpressing METTL3 (Lv-METTL3) or control (Lv-Ctrl) were suspended in 100?uL phosphate-buffered saline (PBS), and were subcutaneously injected into mouse lower right flank. Drug treatment started in the Lv-METTL3 group when the tumour volume reached around 100 mm3. Mice were randomly divided into three groups to receive vehicle, GSK2536771 (30 mg/kg) or rapamycin (1 mg/kg). Drugs were administrated daily through intraperitoneal injection for 18 days. Treatment conditions were chosen as previously reported.
Renal cell carcinoma [ICD-11: 2C90]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [2]
Response Summary Knockdown of METTL3 could obviously promote cell proliferation, migration and invasion function, and induce G0/G1 arrest,METTL3 acts as a novel marker for tumorigenesis, development and survival of RCC. Knockdown of METTL3 promoted changes in pI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) markers' expression with a gain in p-PI3k, p-AKT, p-mTOR and p-p70, and a loss of p-4EBP1.
Responsed Disease Renal cell carcinoma [ICD-11: 2C90]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Down regulation
Cell Process Epithelial-to-mesenchymal transition
Arrest cell cycle at G0/G1 phase
In-vitro Model ACHN Papillary renal cell carcinoma Homo sapiens CVCL_1067
Caki-1 Clear cell renal cell carcinoma Homo sapiens CVCL_0234
Caki-2 Papillary renal cell carcinoma Homo sapiens CVCL_0235
HK2 Normal Acipenser baerii CVCL_YE28
In-vivo Model Cells (5×106 cells in 200 uL) were suspended with 100 uL PBS and 100 uL Matrigel Matrix, and injected subcutaneously into the left armpit of each mouse.
Retina cancer [ICD-11: 2D02]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [3]
Response Summary METTL3 promotes the progression of retinoblastoma through PI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) pathways in vitro and in vivo. METTL3 has an impact on the PI3K-AKT-mTOR-P70S6K/4EBP1 pathway. The cell proliferation results show that the stimulatory function of METTL3 is lost after rapamycin treatment.
Responsed Disease Retinoblastoma [ICD-11: 2D02.2]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Pathway Response PI3K-Akt signaling pathway hsa04151
mTOR signaling pathway hsa04150
Cell Process Cell proliferation
Cell migration
Cell invasion
Cell apoptosis
In-vitro Model WERI-Rb-1 Retinoblastoma Homo sapiens CVCL_1792
Y-79 Retinoblastoma Homo sapiens CVCL_1893
In-vivo Model To establish a subcutaneous tumour model in nude mice, 2 × 107 Y79 cells (METTL3 knockdown group: shNC, shRNA1 and shRNA2; METTL3 up-regulated group: NC and METLL3) were resuspended in 1 mL of pre-cooled PBS, and 200 uL of the cell suspension was injected subcutaneously into the left side of the armpit to investigate tumour growth (4 × 106 per mouse).
Non-alcoholic fatty liver disease [ICD-11: DB92]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [4]
Response Summary The contribution of METTL3-mediated m6A modification of Ddit4 mRNA to macrophage metabolic reprogramming in non-alcoholic fatty liver disease and obesity. In METTL3-deficient macrophages, there is a significant downregulation of Serine/threonine-protein kinase mTOR (MTOR) and nuclear factor Kappa-B (NF-Kappa-B) pathway activity in response to cellular stress and cytokine stimulation, which can be restored by knockdown of DDIT4.
Responsed Disease Non-alcoholic fatty liver disease [ICD-11: DB92]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Pathway Response mTOR signaling pathway hsa04150
HIF-1 signaling pathway hsa04066
In-vivo Model The 8-10 weeks old mice were fed either a high fat diet or HF-CDAA , ad lib for 6-12 weeks. Chow diet was used as control for HFD.The mouse liver was perfused with PBS through portal vein, and liver tissue was cut into small pieces by a scissor. The single cell was made using syringe plunger to mull the tissue, and passed through a 40 uM cell strainer.
Asparagine inhibitor [Approved]
In total 2 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Responsed Disease Colorectal cancer ICD-11: 2B91
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 2 Reporting the m6A-centered Drug Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulator YTH domain-containing family protein 2 (YTHDF2) READER
Target Regulation Up regulation
Responsed Disease Colorectal cancer ICD-11: 2B91
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Chloroquine [Approved]
In total 2 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Responsed Disease Colorectal cancer ICD-11: 2B91
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 2 Reporting the m6A-centered Drug Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulator YTH domain-containing family protein 2 (YTHDF2) READER
Target Regulation Up regulation
Responsed Disease Colorectal cancer ICD-11: 2B91
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Meclofenamate sodium [Approved]
In total 2 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Responsed Disease Colorectal cancer ICD-11: 2B91
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 2 Reporting the m6A-centered Drug Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulator YTH domain-containing family protein 2 (YTHDF2) READER
Target Regulation Up regulation
Responsed Disease Colorectal cancer ICD-11: 2B91
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Rapamycin [Approved]
In total 2 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Responsed Disease Colorectal cancer ICD-11: 2B91
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 2 Reporting the m6A-centered Drug Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulator YTH domain-containing family protein 2 (YTHDF2) READER
Target Regulation Up regulation
Responsed Disease Colorectal cancer ICD-11: 2B91
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
CB-839 [Phase 2]
In total 2 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Responsed Disease Colorectal cancer ICD-11: 2B91
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 2 Reporting the m6A-centered Drug Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulator YTH domain-containing family protein 2 (YTHDF2) READER
Target Regulation Up regulation
Responsed Disease Colorectal cancer ICD-11: 2B91
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
GLS-IN-968 [Investigative]
In total 2 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Responsed Disease Colorectal cancer ICD-11: 2B91
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Experiment 2 Reporting the m6A-centered Drug Response [6]
Response Summary In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition.
Target Regulator YTH domain-containing family protein 2 (YTHDF2) READER
Target Regulation Up regulation
Responsed Disease Colorectal cancer ICD-11: 2B91
Pathway Response mTOR signaling pathway hsa04150
Autophagy hsa04140
Cell Process RNA decay
Cell growth and death
Cell autophagy
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
References
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Ref 2 The M6A methyltransferase METTL3: acting as a tumor suppressor in renal cell carcinoma. Oncotarget. 2017 Oct 10;8(56):96103-96116. doi: 10.18632/oncotarget.21726. eCollection 2017 Nov 10.
Ref 3 m(6)A methyltransferase METTL3 promotes retinoblastoma progression via PI3K/AKT/mTOR pathway. J Cell Mol Med. 2020 Oct 8;24(21):12368-78. doi: 10.1111/jcmm.15736. Online ahead of print.
Ref 4 m(6)A mRNA methylation-directed myeloid cell activation controls progression of NAFLD and obesity. Cell Rep. 2021 Nov 9;37(6):109968. doi: 10.1016/j.celrep.2021.109968.
Ref 5 YTHDF1 promotes hepatocellular carcinoma progression via activating PI3K/AKT/mTOR signaling pathway and inducing epithelial-mesenchymal transition. Exp Hematol Oncol. 2021 Jun 4;10(1):35. doi: 10.1186/s40164-021-00227-0.
Ref 6 Targeting ATF4-dependent pro-survival autophagy to synergize glutaminolysis inhibition. Theranostics. 2021 Jul 25;11(17):8464-8479. doi: 10.7150/thno.60028. eCollection 2021.
Ref 7 The m6A methyltransferase METTL14 inhibits the proliferation, migration, and invasion of gastric cancer by regulating the PI3K/AKT/mTOR signaling pathway. J Clin Lab Anal. 2021 Mar;35(3):e23655. doi: 10.1002/jcla.23655. Epub 2020 Dec 12.