Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05023
[1]
Non-coding RNA ZEB1-AS1 ELAVL1  lncRNA       miRNA   circRNA Direct Enhancement m6A modification ZEB1 ZEB1 ELAVL1 : m6A sites
m6A Modification:
m6A Regulator ELAV-like protein 1 (ELAVL1) READER
m6A Target Zinc finger E-box-binding homeobox 1 (ZEB1)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator ZEB1 antisense RNA 1 (ZEB1-AS1) LncRNA View Details
Regulated Target ELAV-like protein 1 (HuR/ELAVL1) View Details
Crosstalk Relationship ncRNA  →  m6A Enhancement
Crosstalk Mechanism ncRNAs directly impacts m6A modification through recruiting m6A regulator
Crosstalk Summary Zinc finger E-box-binding homeobox 1 (ZEB1) induced-upregulation of ZEB1-AS1 maintained the stability of ZEB1 mRNA by binding with ELAVL1, which formed a feedback loop to facilitate TNBC progression. These findings might provide a new target for TNBC treatment.
Responsed Disease Triple-negative breast cancer ICD-11: 2C6Z
In-vitro Model
MDA-MB-436 Invasive breast carcinoma of no special type Homo sapiens CVCL_0623
MDA-MB-453 Breast adenocarcinoma Homo sapiens CVCL_0418
MCF-7 Invasive breast carcinoma Homo sapiens CVCL_0031
MDA-MB-231 Breast adenocarcinoma Homo sapiens CVCL_0062
In-vivo Model As previously described, Xenograft in vivo mice assay was performed.13 Transfected MDA-MB-436 or MDA-MB-453 cells with sh-ZEB1-AS1#1 or NC (sh-NC) were subcutaneously injected into mice. Every 3 days, tumor growth was monitored.
References
Ref 1 ZEB1 induced-upregulation of long noncoding RNA ZEB1-AS1 facilitates the progression of triple negative breast cancer by binding with ELAVL1 to maintain the stability of ZEB1 mRNA. J Cell Biochem. 2020 Oct;121(10):4176-4187. doi: 10.1002/jcb.29572. Epub 2020 Jan 10.