m6A Target Gene Information

General Information of the m6A Target Gene (ID: M6ATAR00410)
Target Name Sequestosome-1 (SQSTM1)
Synonyms
EBI3-associated protein of 60 kDa; EBIAP; p60; Phosphotyrosine-independent ligand for the Lck SH2 domain of 62 kDa; Ubiquitin-binding protein p62; ORCA; OSIL
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Gene Name SQSTM1
Chromosomal Location 5q35.3
Function
Autophagy receptor required for selective macroautophagy (aggrephagy). Functions as a bridge between polyubiquitinated cargo and autophagosomes. Interacts directly with both the cargo to become degraded and an autophagy modifier of the MAP1 LC3 family . Along with WDFY3, involved in the formation and autophagic degradation of cytoplasmic ubiquitin-containing inclusions (p62 bodies, ALIS/aggresome-like induced structures). Along with WDFY3, required to recruit ubiquitinated proteins to PML bodies in the nucleus. May regulate the activation of NFKB1 by TNF-alpha, nerve growth factor (NGF) and interleukin-1. May play a role in titin/TTN downstream signaling in muscle cells. May regulate signaling cascades through ubiquitination. Adapter that mediates the interaction between TRAF6 and CYLD (By similarity). May be involved in cell differentiation, apoptosis, immune response and regulation of K(+) channels. Involved in endosome organization by retaining vesicles in the perinuclear cloud: following ubiquitination by RNF26, attracts specific vesicle-associated adapters, forming a molecular bridge that restrains cognate vesicles in the perinuclear region and organizes the endosomal pathway for efficient cargo transport. Promotes relocalization of 'Lys-63'-linked ubiquitinated STING1 to autophagosomes. Acts as an activator of the NFE2L2/NRF2 pathway via interaction with KEAP1: interaction inactivates the BCR(KEAP1) complex, promoting nuclear accumulation of NFE2L2/NRF2 and subsequent expression of cytoprotective genes.
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Gene ID 8878
Uniprot ID
SQSTM_HUMAN
HGNC ID
HGNC:11280
Ensembl Gene ID
ENSG00000161011
KEGG ID
hsa:8878
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
SQSTM1 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]
 Regulator Info 
Representative RNA-seq result indicating the expression of this target gene regulated by METTL3
Cell Line HUVEC cell line Homo sapiens
Treatment: shMETTL3 HUVEC cells
Control: shScramble HUVEC cells
 GSE157544
Regulation
logFC: -6.28E-01
p-value: 1.94E-05
More Results Click to View More RNA-seq Results
Representative RIP-seq result supporting the interaction between SQSTM1 and the regulator
Cell Line MDA-MB-231 Homo sapiens
Regulation logFC: 2.03E+00 GSE60213
In total 3 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and Sequestosome-1 (SQSTM1). beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance.
Target Regulation Up regulation
Responsed Disease Non-small-cell lung carcinoma ICD-11: 2C25.Y
 Disease Info 
Responsed Drug Chloroquine Approved
 Drug Info 
Pathway Response Autophagy hsa04140
Cell Process Autophagic lysosome acidification
In-vitro Model Gefitinib-resistant cell line HCC827GR (Gefitinib-resistant HCC827 cell line)
Gefitinib-resistant cell line PC9GR (Gefitinib-resistant PC9 cell line)
HCC827 Lung adenocarcinoma Homo sapiens CVCL_2063
PC-9 Lung adenocarcinoma Homo sapiens CVCL_B260
In-vivo Model NSCLC gefitinib-resistant cells (5 × 106 cells in 100 uL PBS) were injected subcutaneously into the lateral surface of the left abdomen of 6-week-old female BALB/c nude mice (at least five mice per group to ensure accuracy).
Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and Sequestosome-1 (SQSTM1). beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance.
Target Regulation Up regulation
Responsed Disease Non-small-cell lung carcinoma ICD-11: 2C25.Y
 Disease Info 
Responsed Drug Gefitinib Approved
 Drug Info 
Pathway Response Autophagy hsa04140
Cell Process Autophagic lysosome acidification
In-vitro Model Gefitinib-resistant cell line HCC827GR (Gefitinib-resistant HCC827 cell line)
Gefitinib-resistant cell line PC9GR (Gefitinib-resistant PC9 cell line)
HCC827 Lung adenocarcinoma Homo sapiens CVCL_2063
PC-9 Lung adenocarcinoma Homo sapiens CVCL_B260
In-vivo Model NSCLC gefitinib-resistant cells (5 × 106 cells in 100 uL PBS) were injected subcutaneously into the lateral surface of the left abdomen of 6-week-old female BALB/c nude mice (at least five mice per group to ensure accuracy).
Experiment 3 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and Sequestosome-1 (SQSTM1). beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance.
Target Regulation Up regulation
Responsed Disease Non-small-cell lung carcinoma ICD-11: 2C25.Y
 Disease Info 
Responsed Drug Beta-Elemen Phase 3
 Drug Info 
Pathway Response Autophagy hsa04140
Cell Process Autophagic lysosome acidification
In-vitro Model Gefitinib-resistant cell line HCC827GR (Gefitinib-resistant HCC827 cell line)
Gefitinib-resistant cell line PC9GR (Gefitinib-resistant PC9 cell line)
HCC827 Lung adenocarcinoma Homo sapiens CVCL_2063
PC-9 Lung adenocarcinoma Homo sapiens CVCL_B260
In-vivo Model NSCLC gefitinib-resistant cells (5 × 106 cells in 100 uL PBS) were injected subcutaneously into the lateral surface of the left abdomen of 6-week-old female BALB/c nude mice (at least five mice per group to ensure accuracy).
Fat mass and obesity-associated protein (FTO) [ERASER]
 Regulator Info 
Representative RNA-seq result indicating the expression of this target gene regulated by FTO
Cell Line 253J cell line Homo sapiens
Treatment: siFTO 253J cells
Control: 253J cells
 GSE150239
Regulation
logFC: 6.53E-01
p-value: 1.38E-07
More Results Click to View More RNA-seq Results
In total 3 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [2]
Response Summary The m6A changes caused by FTO influence the stability of ULK1 transcripts, likely through a YTHDF2-dependent manner.Under both basal and rapamycin-induced autophagy conditions, depletion of FTO significantly reduced the formation of GFP-LC3B puncta. The level of Sequestosome-1 (SQSTM1)/SQSTM1 (an autophagy substrate) was higher in FTO-knockdown cells than that in control cells. FTO specifically upregulates the ULK1 protein abundance. ULK1 mRNA undergoes m6A modification in the 3'-UTR and the m6A-marked ULK1 transcripts can further be targeted for degradation by YTHDF2.
Target Regulation Down regulation
Pathway Response Autophagy hsa04140
Cell Process RNA stability
Cell autophagy
In-vitro Model HEK293T Normal Homo sapiens CVCL_0063
HeLa Endocervical adenocarcinoma Homo sapiens CVCL_0030
Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene [3]
Response Summary FTO deletion inhibited arsenic-induced tumorigenesis. Epidermis-specific FTO deletion prevented skin tumorigenesis induced by arsenic and UVB irradiation. NEDD4L was identified as the m6A-modified gene target of FTO. Arsenic stabilizes FTO protein through inhibiting Sequestosome-1 (SQSTM1)-mediated selective autophagy. FTO-mediated dysregulation of mRNA m6A methylation as an epitranscriptomic mechanism to promote arsenic tumorigenicity. Arsenic suppresses p62 expression by downregulating the NF-Kappa-B pathway to upregulate FTO.
Target Regulation Down regulation
Responsed Disease Solid tumour/cancer ICD-11: 2A00-2F9Z
 Disease Info 
Pathway Response Autophagy hsa04140
Cell Process Cellular Processes, Transport and catabolism
Cell autophagy
In-vitro Model HaCaT Normal Homo sapiens CVCL_0038
HEK293T Normal Homo sapiens CVCL_0063
HeLa Endocervical adenocarcinoma Homo sapiens CVCL_0030
MEF (Mouse embryonic fibroblasts)
In-vivo Model As cells (5 million) in Matrigel or As-T (1 million) cells in PBS with or without gene manipulations were injected subcutaneously into the right flanks of female mice (6-8 weeks of age). For treatment with CS1 or CS2, As-T cells (1 million) in PBS were injected subcutaneously into the right flanks of 6-week-old female nude mice.
Experiment 3 Reporting the m6A Methylation Regulator of This Target Gene [3]
Response Summary FTO deletion inhibited arsenic-induced tumorigenesis. Epidermis-specific FTO deletion prevented skin tumorigenesis induced by arsenic and UVB irradiation. NEDD4L was identified as the m6A-modified gene target of FTO. Arsenic stabilizes FTO protein through inhibiting Sequestosome-1 (SQSTM1)-mediated selective autophagy. FTO-mediated dysregulation of mRNA m6A methylation as an epitranscriptomic mechanism to promote arsenic tumorigenicity. Arsenic suppresses p62 expression by downregulating the NF-Kappa-B pathway to upregulate FTO.
Target Regulation Down regulation
Responsed Disease Human skin lesions ICD-11: ME60
 Disease Info 
Pathway Response Autophagy hsa04140
Cell Process Cellular Processes, Transport and catabolism
Cell autophagy
In-vitro Model HaCaT Normal Homo sapiens CVCL_0038
HEK293T Normal Homo sapiens CVCL_0063
HeLa Endocervical adenocarcinoma Homo sapiens CVCL_0030
MEF (Mouse embryonic fibroblasts)
In-vivo Model As cells (5 million) in Matrigel or As-T (1 million) cells in PBS with or without gene manipulations were injected subcutaneously into the right flanks of female mice (6-8 weeks of age). For treatment with CS1 or CS2, As-T cells (1 million) in PBS were injected subcutaneously into the right flanks of 6-week-old female nude mice.
YTH domain-containing protein 1 (YTHDC1) [READER]
 Regulator Info 
Representative RNA-seq result indicating the expression of this target gene regulated by YTHDC1
Cell Line MOLM-13 cell line Homo sapiens
Treatment: shYTHDC1 MOLM13 cells
Control: shControl MOLM13 cells
 GSE168565
Regulation
logFC: 1.02E+00
p-value: 3.33E-09
More Results Click to View More RNA-seq Results
In total 2 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [4]
Response Summary In diabetes/diabetic skin, YTHDC1 interacted and cooperated with ELAVL1/HuR (ELAV like RNA binding protein 1) in modulating the expression of Sequestosome-1 (SQSTM1).
Target Regulation Up regulation
Responsed Disease Diabetes ICD-11: 5A10-5A14
 Disease Info 
Pathway Response Autophagy hsa04140
Cell Process Cellular Processes
Cellular Transport
Cellular catabolism
Cell apoptosis
Cell autophagy
In-vitro Model HaCaT Normal Homo sapiens CVCL_0038
NHEK (Normal human epithelial keratinocytes)
In-vivo Model The WT-si-NC, WT-si-Ythdc1 and WT-si-Sqstm1 groups were intracutaneously injected with corresponding siRNAs (si-NC, si-Ythdc1, or si-Sqstm1, 2.5 nmol) on the circle.
Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene [4]
Response Summary In diabetes/diabetic skin, YTHDC1 interacted and cooperated with ELAVL1/HuR (ELAV like RNA binding protein 1) in modulating the expression of Sequestosome-1 (SQSTM1).
Target Regulation Up regulation
Responsed Disease Diabetic skin lesions ICD-11: EB90.0
 Disease Info 
Pathway Response Autophagy hsa04140
Cell Process Cellular Processes
Cellular Transport
Cellular catabolism
Cell apoptosis
Cell autophagy
In-vitro Model HaCaT Normal Homo sapiens CVCL_0038
NHEK (Normal human epithelial keratinocytes)
In-vivo Model The WT-si-NC, WT-si-Ythdc1 and WT-si-Sqstm1 groups were intracutaneously injected with corresponding siRNAs (si-NC, si-Ythdc1, or si-Sqstm1, 2.5 nmol) on the circle.
Solid tumour/cancer [ICD-11: 2A00-2F9Z]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [3]
Response Summary FTO deletion inhibited arsenic-induced tumorigenesis. Epidermis-specific FTO deletion prevented skin tumorigenesis induced by arsenic and UVB irradiation. NEDD4L was identified as the m6A-modified gene target of FTO. Arsenic stabilizes FTO protein through inhibiting Sequestosome-1 (SQSTM1)-mediated selective autophagy. FTO-mediated dysregulation of mRNA m6A methylation as an epitranscriptomic mechanism to promote arsenic tumorigenicity. Arsenic suppresses p62 expression by downregulating the NF-Kappa-B pathway to upregulate FTO.
Responsed Disease Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
 Regulator Info 
Target Regulation Down regulation
Pathway Response Autophagy hsa04140
Cell Process Cellular Processes, Transport and catabolism
Cell autophagy
In-vitro Model HaCaT Normal Homo sapiens CVCL_0038
HEK293T Normal Homo sapiens CVCL_0063
HeLa Endocervical adenocarcinoma Homo sapiens CVCL_0030
MEF (Mouse embryonic fibroblasts)
In-vivo Model As cells (5 million) in Matrigel or As-T (1 million) cells in PBS with or without gene manipulations were injected subcutaneously into the right flanks of female mice (6-8 weeks of age). For treatment with CS1 or CS2, As-T cells (1 million) in PBS were injected subcutaneously into the right flanks of 6-week-old female nude mice.
Lung cancer [ICD-11: 2C25]
 Disease Info 
In total 3 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and Sequestosome-1 (SQSTM1). beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance.
Responsed Disease Non-small-cell lung carcinoma [ICD-11: 2C25.Y]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Up regulation
Responsed Drug Chloroquine Approved
 Drug Info 
Pathway Response Autophagy hsa04140
Cell Process Autophagic lysosome acidification
In-vitro Model Gefitinib-resistant cell line HCC827GR (Gefitinib-resistant HCC827 cell line)
Gefitinib-resistant cell line PC9GR (Gefitinib-resistant PC9 cell line)
HCC827 Lung adenocarcinoma Homo sapiens CVCL_2063
PC-9 Lung adenocarcinoma Homo sapiens CVCL_B260
In-vivo Model NSCLC gefitinib-resistant cells (5 × 106 cells in 100 uL PBS) were injected subcutaneously into the lateral surface of the left abdomen of 6-week-old female BALB/c nude mice (at least five mice per group to ensure accuracy).
Experiment 2 Reporting the m6A-centered Disease Response [1]
Response Summary METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and Sequestosome-1 (SQSTM1). beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance.
Responsed Disease Non-small-cell lung carcinoma [ICD-11: 2C25.Y]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Up regulation
Responsed Drug Gefitinib Approved
 Drug Info 
Pathway Response Autophagy hsa04140
Cell Process Autophagic lysosome acidification
In-vitro Model Gefitinib-resistant cell line HCC827GR (Gefitinib-resistant HCC827 cell line)
Gefitinib-resistant cell line PC9GR (Gefitinib-resistant PC9 cell line)
HCC827 Lung adenocarcinoma Homo sapiens CVCL_2063
PC-9 Lung adenocarcinoma Homo sapiens CVCL_B260
In-vivo Model NSCLC gefitinib-resistant cells (5 × 106 cells in 100 uL PBS) were injected subcutaneously into the lateral surface of the left abdomen of 6-week-old female BALB/c nude mice (at least five mice per group to ensure accuracy).
Experiment 3 Reporting the m6A-centered Disease Response [1]
Response Summary METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and Sequestosome-1 (SQSTM1). beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance.
Responsed Disease Non-small-cell lung carcinoma [ICD-11: 2C25.Y]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Up regulation
Responsed Drug Beta-Elemen Phase 3
 Drug Info 
Pathway Response Autophagy hsa04140
Cell Process Autophagic lysosome acidification
In-vitro Model Gefitinib-resistant cell line HCC827GR (Gefitinib-resistant HCC827 cell line)
Gefitinib-resistant cell line PC9GR (Gefitinib-resistant PC9 cell line)
HCC827 Lung adenocarcinoma Homo sapiens CVCL_2063
PC-9 Lung adenocarcinoma Homo sapiens CVCL_B260
In-vivo Model NSCLC gefitinib-resistant cells (5 × 106 cells in 100 uL PBS) were injected subcutaneously into the lateral surface of the left abdomen of 6-week-old female BALB/c nude mice (at least five mice per group to ensure accuracy).
Diabetes [ICD-11: 5A10-5A14]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [4]
Response Summary In diabetes/diabetic skin, YTHDC1 interacted and cooperated with ELAVL1/HuR (ELAV like RNA binding protein 1) in modulating the expression of Sequestosome-1 (SQSTM1).
Responsed Disease Diabetes [ICD-11: 5A10-5A14]
Target Regulator YTH domain-containing protein 1 (YTHDC1) READER
 Regulator Info 
Target Regulation Up regulation
Pathway Response Autophagy hsa04140
Cell Process Cellular Processes
Cellular Transport
Cellular catabolism
Cell apoptosis
Cell autophagy
In-vitro Model HaCaT Normal Homo sapiens CVCL_0038
NHEK (Normal human epithelial keratinocytes)
In-vivo Model The WT-si-NC, WT-si-Ythdc1 and WT-si-Sqstm1 groups were intracutaneously injected with corresponding siRNAs (si-NC, si-Ythdc1, or si-Sqstm1, 2.5 nmol) on the circle.
Diabetic skin lesions [ICD-11: EB90]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [4]
Response Summary In diabetes/diabetic skin, YTHDC1 interacted and cooperated with ELAVL1/HuR (ELAV like RNA binding protein 1) in modulating the expression of Sequestosome-1 (SQSTM1).
Responsed Disease Diabetic skin lesions [ICD-11: EB90.0]
Target Regulator YTH domain-containing protein 1 (YTHDC1) READER
 Regulator Info 
Target Regulation Up regulation
Pathway Response Autophagy hsa04140
Cell Process Cellular Processes
Cellular Transport
Cellular catabolism
Cell apoptosis
Cell autophagy
In-vitro Model HaCaT Normal Homo sapiens CVCL_0038
NHEK (Normal human epithelial keratinocytes)
In-vivo Model The WT-si-NC, WT-si-Ythdc1 and WT-si-Sqstm1 groups were intracutaneously injected with corresponding siRNAs (si-NC, si-Ythdc1, or si-Sqstm1, 2.5 nmol) on the circle.
Human skin lesions [ICD-11: ME60]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [3]
Response Summary FTO deletion inhibited arsenic-induced tumorigenesis. Epidermis-specific FTO deletion prevented skin tumorigenesis induced by arsenic and UVB irradiation. NEDD4L was identified as the m6A-modified gene target of FTO. Arsenic stabilizes FTO protein through inhibiting Sequestosome-1 (SQSTM1)-mediated selective autophagy. FTO-mediated dysregulation of mRNA m6A methylation as an epitranscriptomic mechanism to promote arsenic tumorigenicity. Arsenic suppresses p62 expression by downregulating the NF-Kappa-B pathway to upregulate FTO.
Responsed Disease Human skin lesions [ICD-11: ME60]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
 Regulator Info 
Target Regulation Down regulation
Pathway Response Autophagy hsa04140
Cell Process Cellular Processes, Transport and catabolism
Cell autophagy
In-vitro Model HaCaT Normal Homo sapiens CVCL_0038
HEK293T Normal Homo sapiens CVCL_0063
HeLa Endocervical adenocarcinoma Homo sapiens CVCL_0030
MEF (Mouse embryonic fibroblasts)
In-vivo Model As cells (5 million) in Matrigel or As-T (1 million) cells in PBS with or without gene manipulations were injected subcutaneously into the right flanks of female mice (6-8 weeks of age). For treatment with CS1 or CS2, As-T cells (1 million) in PBS were injected subcutaneously into the right flanks of 6-week-old female nude mice.
Chloroquine [Approved]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response [1]
Response Summary METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and Sequestosome-1 (SQSTM1). beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance.
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Up regulation
Responsed Disease Non-small-cell lung carcinoma ICD-11: 2C25.Y
 Disease Info 
Pathway Response Autophagy hsa04140
Cell Process Autophagic lysosome acidification
In-vitro Model Gefitinib-resistant cell line HCC827GR (Gefitinib-resistant HCC827 cell line)
Gefitinib-resistant cell line PC9GR (Gefitinib-resistant PC9 cell line)
HCC827 Lung adenocarcinoma Homo sapiens CVCL_2063
PC-9 Lung adenocarcinoma Homo sapiens CVCL_B260
In-vivo Model NSCLC gefitinib-resistant cells (5 × 106 cells in 100 uL PBS) were injected subcutaneously into the lateral surface of the left abdomen of 6-week-old female BALB/c nude mice (at least five mice per group to ensure accuracy).
Gefitinib [Approved]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response [1]
Response Summary METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and Sequestosome-1 (SQSTM1). beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance.
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Up regulation
Responsed Disease Non-small-cell lung carcinoma ICD-11: 2C25.Y
 Disease Info 
Pathway Response Autophagy hsa04140
Cell Process Autophagic lysosome acidification
In-vitro Model Gefitinib-resistant cell line HCC827GR (Gefitinib-resistant HCC827 cell line)
Gefitinib-resistant cell line PC9GR (Gefitinib-resistant PC9 cell line)
HCC827 Lung adenocarcinoma Homo sapiens CVCL_2063
PC-9 Lung adenocarcinoma Homo sapiens CVCL_B260
In-vivo Model NSCLC gefitinib-resistant cells (5 × 106 cells in 100 uL PBS) were injected subcutaneously into the lateral surface of the left abdomen of 6-week-old female BALB/c nude mice (at least five mice per group to ensure accuracy).
Beta-Elemen [Phase 3]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response [1]
Response Summary METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and Sequestosome-1 (SQSTM1). beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance.
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Up regulation
Responsed Disease Non-small-cell lung carcinoma ICD-11: 2C25.Y
 Disease Info 
Pathway Response Autophagy hsa04140
Cell Process Autophagic lysosome acidification
In-vitro Model Gefitinib-resistant cell line HCC827GR (Gefitinib-resistant HCC827 cell line)
Gefitinib-resistant cell line PC9GR (Gefitinib-resistant PC9 cell line)
HCC827 Lung adenocarcinoma Homo sapiens CVCL_2063
PC-9 Lung adenocarcinoma Homo sapiens CVCL_B260
In-vivo Model NSCLC gefitinib-resistant cells (5 × 106 cells in 100 uL PBS) were injected subcutaneously into the lateral surface of the left abdomen of 6-week-old female BALB/c nude mice (at least five mice per group to ensure accuracy).
References
Ref 1 The mechanism of m(6)A methyltransferase METTL3-mediated autophagy in reversing gefitinib resistance in NSCLC cells by Beta-elemene. Cell Death Dis. 2020 Nov 11;11(11):969. doi: 10.1038/s41419-020-03148-8.
Ref 2 m(6)A RNA modification controls autophagy through upregulating ULK1 protein abundance. Cell Res. 2018 Sep;28(9):955-957. doi: 10.1038/s41422-018-0069-8. Epub 2018 Jul 25.
Ref 3 Autophagy of the m(6)A mRNA demethylase FTO is impaired by low-level arsenic exposure to promote tumorigenesis. Nat Commun. 2021 Apr 12;12(1):2183. doi: 10.1038/s41467-021-22469-6.
Ref 4 m(6)A reader YTHDC1 modulates autophagy by targeting SQSTM1 in diabetic skin. Autophagy. 2022 Jun;18(6):1318-1337. doi: 10.1080/15548627.2021.1974175. Epub 2021 Oct 17.