Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00630
[1], [2], [3]
m6A modification hsa-mir-146a hsa-mir-146a METTL14 Methylation : m6A sites Indirect Enhancement RNA modification BRCA1 BRCA1 ALYREF : modification sites
m6A Modification:
m6A Regulator Methyltransferase-like 14 (METTL14) WRITER
m6A Target hsa-mir-146a
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type RNA modification (RNAMod)  >> 5-methylcytidine (m5C)
Epigenetic Regulator THO complex subunit 4 (ALYREF) READER View Details
Regulated Target Breast cancer type 1 susceptibility protein (BRCA1) View Details
Crosstalk Relationship m6A  →  m5C Enhancement
Crosstalk Mechanism m6A modification indirectly impacts RNA modification through downstream signaling pathways
Crosstalk Summary METTL14 interacts with hsa-mir-146a, reading its m6A level and promoting its physical interaction with Breast cancer type 1 susceptibility protein (BRCA1), which was regulated by ALYREF-mediated m5C modification.
In-vitro Model
HeLa Endocervical adenocarcinoma Homo sapiens CVCL_0030
MDA-MB-231 Breast adenocarcinoma Homo sapiens CVCL_0062
MCF-7 Invasive breast carcinoma Homo sapiens CVCL_0031
References
Ref 1 Suppression of DDX39B sensitizes ovarian cancer cells to DNA-damaging chemotherapeutic agents via destabilizing BRCA1 mRNA. Oncogene. 2020 Nov;39(47):7051-7062. doi: 10.1038/s41388-020-01482-x. Epub 2020 Sep 28.
Ref 2 METTL14 promotes the migration and invasion of breast cancer cells by modulating N6?methyladenosine and hsa?miR?146a?5p expression. Oncol Rep. 2020 May;43(5):1375-1386. doi: 10.3892/or.2020.7515. Epub 2020 Feb 24.
Ref 3 Targeting MALAT1 induces DNA damage and sensitize non-small cell lung cancer cells to cisplatin by repressing BRCA1. Cancer Chemother Pharmacol. 2020 Nov;86(5):663-672. doi: 10.1007/s00280-020-04152-7. Epub 2020 Oct 8.