General Information of the m6A Target Gene (ID: M6ATAR00118)
Target Name microRNA 375 (MIR375)
Synonyms
MIR375; MIRN375; hsa-mir-375
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Gene Name MIR375
Chromosomal Location 2q35
Family MicroRNAs
Gene ID 494324
HGNC ID
HGNC:31868
miRBase ID
MI0000783
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
MIR375 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).
Browse Regulator
Browse Disease
Methyltransferase-like 14 (METTL14) [WRITER]
In total 2 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary METTL14 suppressed Colorectal cancer cell growth, migration, and invasion via the microRNA 375 (MIR375)/YAP1 and miR-375/SP1 pathways.
Target Regulation Up regulation
Responsed Disease Colorectal cancer ICD-11: 2B91
Pathway Response Hippo signaling pathway hsa04390
Cell Process Cell growth and metastasis
In-vitro Model DLD-1 Colon adenocarcinoma Homo sapiens CVCL_0248
FHC Normal Homo sapiens CVCL_3688
HCT 116 Colon carcinoma Homo sapiens CVCL_0291
HCT 8 Colon adenocarcinoma Homo sapiens CVCL_2478
HT29 Colon cancer Mus musculus CVCL_A8EZ
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
SW620 Colon adenocarcinoma Homo sapiens CVCL_0547
In-vivo Model Six-week-old BALB/c nude mice were purchased from the College of Veterinary Medicine, Yang Zhou University. For the xenografted tumor model, 1 × 107 HCT116 cells in 0.2 mL PBS were subcutaneously injected into BALB/c nude mice, which were randomly divided into four groups (six mice per group). The volume of the tumors was calculated with the following equation: V = 0.5 × (length × width2). For metastasis experiments, 2 × 106 cells in 0.2 mL PBS were injected into the tail vein of nude mice, which were randomly divided into four groups (six mice per group).
Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene [3]
Response Summary Mettl14-mediated m6A modification inhibited RASD1 and induced the apoptosis of spinal cord neurons in SCI by promoting the transformation of pri-miR-375 to mature microRNA 375 (MIR375).
Target Regulation Up regulation
Responsed Disease Injuries of spine or trunk ICD-11: ND51
Pathway Response mTOR signaling pathway hsa04150
In-vitro Model C8-D1A Normal Mus musculus CVCL_6379
C8-B4 Normal Mus musculus CVCL_6378
In-vivo Model An incision was made in the skin along the medial dorsal line to the aponeurotic and muscular planes, and the posterior vertebral arches were exposed from T8 to T12. Under the dissection stereomicroscope, 3-mm-long laminectomy was performed on the caudal end of T10 vertebra and the rostral end of T11 vertebra. The Infinite Horizons impactor (Infinite Horizons, L.L.C., Lexington, KY, USA) was adopted to produce the contusion SCI using a force of 60 kdyn/cm2. The SCI model rats were established and randomly assigned to SCI model group, ant-NC (negative control, SCI rats treated with lentiviral (lv)-shRNA NC of Mettl14) group and ant-Mettl14 group (SCI rats treated with lv-shRNA of Mettl14). Rats were subjected to laminectomy and then treated with lv-shRNA Mettl14/lv-shRNA-NC (50 ul/day, 100 nmoL/mL; RiboBio, Guangzhou, China) via an intrathecal injection through lumbar puncture for 3 days (0, 1, and 2 days) after 15 min of SCI modelling. In addition, the unmodeled rats were set as sham group.
Colorectal cancer [ICD-11: 2B91]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary METTL14 suppressed Colorectal cancer cell growth, migration, and invasion via the microRNA 375 (MIR375)/YAP1 and miR-375/SP1 pathways.
Responsed Disease Colorectal cancer [ICD-11: 2B91]
Target Regulator Methyltransferase-like 14 (METTL14) WRITER
Target Regulation Up regulation
Pathway Response Hippo signaling pathway hsa04390
Cell Process Cell growth and metastasis
In-vitro Model DLD-1 Colon adenocarcinoma Homo sapiens CVCL_0248
FHC Normal Homo sapiens CVCL_3688
HCT 116 Colon carcinoma Homo sapiens CVCL_0291
HCT 8 Colon adenocarcinoma Homo sapiens CVCL_2478
HT29 Colon cancer Mus musculus CVCL_A8EZ
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
SW620 Colon adenocarcinoma Homo sapiens CVCL_0547
In-vivo Model Six-week-old BALB/c nude mice were purchased from the College of Veterinary Medicine, Yang Zhou University. For the xenografted tumor model, 1 × 107 HCT116 cells in 0.2 mL PBS were subcutaneously injected into BALB/c nude mice, which were randomly divided into four groups (six mice per group). The volume of the tumors was calculated with the following equation: V = 0.5 × (length × width2). For metastasis experiments, 2 × 106 cells in 0.2 mL PBS were injected into the tail vein of nude mice, which were randomly divided into four groups (six mice per group).
Injuries of spine or trunk [ICD-11: ND51]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [3]
Response Summary Mettl14-mediated m6A modification inhibited RASD1 and induced the apoptosis of spinal cord neurons in SCI by promoting the transformation of pri-miR-375 to mature microRNA 375 (MIR375).
Responsed Disease Injuries of spine or trunk [ICD-11: ND51]
Target Regulator Methyltransferase-like 14 (METTL14) WRITER
Target Regulation Up regulation
Pathway Response mTOR signaling pathway hsa04150
In-vitro Model C8-D1A Normal Mus musculus CVCL_6379
C8-B4 Normal Mus musculus CVCL_6378
In-vivo Model An incision was made in the skin along the medial dorsal line to the aponeurotic and muscular planes, and the posterior vertebral arches were exposed from T8 to T12. Under the dissection stereomicroscope, 3-mm-long laminectomy was performed on the caudal end of T10 vertebra and the rostral end of T11 vertebra. The Infinite Horizons impactor (Infinite Horizons, L.L.C., Lexington, KY, USA) was adopted to produce the contusion SCI using a force of 60 kdyn/cm2. The SCI model rats were established and randomly assigned to SCI model group, ant-NC (negative control, SCI rats treated with lentiviral (lv)-shRNA NC of Mettl14) group and ant-Mettl14 group (SCI rats treated with lv-shRNA of Mettl14). Rats were subjected to laminectomy and then treated with lv-shRNA Mettl14/lv-shRNA-NC (50 ul/day, 100 nmoL/mL; RiboBio, Guangzhou, China) via an intrathecal injection through lumbar puncture for 3 days (0, 1, and 2 days) after 15 min of SCI modelling. In addition, the unmodeled rats were set as sham group.
Full List of Crosstalk(s) between m6A Modification and Epigenetic Regulation Related to This Regulator
RNA modification
m6A Regulator: Methyltransferase-like 14 (METTL14)
In total 6 item(s) under this m6A regulator
Crosstalk ID: M6ACROT00657
Epigenetic Regulator Y-box-binding protein 1 (YBX1)
Regulated Target Hypoxia-inducible factor 1-alpha (HIF-1-Alpha/HIF1A)
Crosstalk relationship m6A → m5C
Crosstalk ID: M6ACROT00658
Epigenetic Regulator H/ACA ribonucleoprotein complex subunit DKC1 (DKC1)
Regulated Target Hypoxia-inducible factor 1-alpha (HIF-1-Alpha/HIF1A)
Crosstalk relationship m6A → Pseudouridine
Crosstalk ID: M6ACROT00659
Epigenetic Regulator Y-box-binding protein 1 (YBX1)
Regulated Target Transcriptional coactivator YAP1 (YAP1)
Crosstalk relationship m6A → m5C
Crosstalk ID: M6ACROT00660
Epigenetic Regulator Fat mass and obesity-associated protein (FTO)
Regulated Target NAD-dependent protein deacetylase sirtuin-1 (SIRT1)
Crosstalk relationship m6A → m6Am
Crosstalk ID: M6ACROT00661
Epigenetic Regulator Fat mass and obesity-associated protein (FTO)
Regulated Target Metastasis associated lung adenocarcinoma transcript 1 (MALAT1)
Crosstalk relationship m6Am → m6A
Crosstalk ID: M6ACROT00662
Epigenetic Regulator Methyltransferase-like protein 1 (METTL1)
Regulated Target High mobility group protein HMGI-C (HMGA2)
Crosstalk relationship m6A → m7G
DNA modification
m6A Regulator: Methyltransferase-like 14 (METTL14)
In total 3 item(s) under this m6A regulator
Crosstalk ID: M6ACROT02101
Epigenetic Regulator Cysteine methyltransferase DNMT3A (DNMT3A)
Regulated Target Methyltransferase-like protein 14 (METTL14)
Crosstalk relationship DNA modification → m6A
Disease Breast cancer
Crosstalk ID: M6ACROT02102
Epigenetic Regulator DNA (cytosine-5)-methyltransferase 3B (DNMT3B)
Regulated Target Methyltransferase-like protein 14 (METTL14)
Crosstalk relationship DNA modification → m6A
Disease Breast cancer
Crosstalk ID: M6ACROT02103
Epigenetic Regulator DNA (cytosine-5)-methyltransferase 1 (DNMT1)
Regulated Target Methyltransferase-like protein 14 (METTL14)
Crosstalk relationship DNA modification → m6A
Disease Breast cancer
Histone modification
m6A Regulator: Methyltransferase-like 14 (METTL14)
In total 1 item(s) under this m6A regulator
Crosstalk ID: M6ACROT03276
Epigenetic Regulator Lysine-specific demethylase 5C (KDM5C)
Regulated Target Histone H3 lysine 4 trimethylation (H3K4me3)
Crosstalk relationship Histone modification → m6A
Disease Colorectal cancer
Non-coding RNA
m6A Regulator: Methyltransferase-like 14 (METTL14)
In total 3 item(s) under this m6A regulator
Crosstalk ID: M6ACROT05410
Epigenetic Regulator MicroRNA 375 (MIR375)
Crosstalk relationship m6A → ncRNA
Disease Colorectal cancer
Crosstalk ID: M6ACROT05606
Epigenetic Regulator MicroRNA 375 (MIR375)
Regulated Target Dexamethasone-induced Ras-related protein 1 (RASD1)
Crosstalk relationship m6A → ncRNA
Disease Injuries of spine or trunk
Crosstalk ID: M6ACROT05931
Epigenetic Regulator MicroRNA 375 (MIR375)
Regulated Target Transcription factor SOX-12 (SOX12)
Crosstalk relationship m6A → ncRNA
Disease Breast cancer
References
Ref 1 RETRACTED: METTL14 Suppresses CRC Progression via Regulating N6-Methyladenosine-Dependent Primary miR-375 Processing. Mol Ther. 2020 Feb 5;28(2):599-612. doi: 10.1016/j.ymthe.2019.11.016. Epub 2019 Nov 20.
Ref 2 Suradista NSC 651016 inhibits the angiogenic activity of CXCL12-stromal cell-derived factor 1alpha. Clin Cancer Res. 2002 Dec;8(12):3955-60.
Ref 3 Mettl14-mediated m6A modification modulates neuron apoptosis during the repair of spinal cord injury by regulating the transformation from pri-mir-375 to miR-375. Cell Biosci. 2021 Mar 11;11(1):52. doi: 10.1186/s13578-020-00526-9.