Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05016
[1], [2]
Non-coding RNA DARS-AS1 IGF2BP3  lncRNA       miRNA   circRNA Direct Enhancement m6A modification ACIN1 ACIN1 IGF2BP3 : m6A sites
m6A Modification:
m6A Regulator Insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) READER
m6A Target Apoptotic chromatin condensation inducer in the nucleus (ACIN1)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator DARS1 antisense RNA 1 (DARS1-AS1) LncRNA View Details
Regulated Target Insulin like growth factor 2 mRNA binding protein 3 (IGF2BP3) View Details
Crosstalk Relationship ncRNA  →  m6A Enhancement
Crosstalk Mechanism ncRNAs directly impacts m6A modification through modulating the expression level of m6A regulator
Crosstalk Summary Downregulation of LncRNA DARS1-AS1 Inhibits the Tumorigenesis of Cervical Cancer via Inhibition of IGF2BP3, METTL3 interacts with IGF2BP3 to promote the mRNA stability of Apoptotic chromatin condensation inducer in the nucleus (ACIN1), the overexpression of which induces the aggressiveness of CC cells.
Responsed Disease Cervical cancer ICD-11: 2C77
Pathway Response mRNA surveillance pathway hsa03015
RNA degradation hsa03018
Cell Process RNA stability
In-vitro Model
SiHa Cervical squamous cell carcinoma Homo sapiens CVCL_0032
HeLa Endocervical adenocarcinoma Homo sapiens CVCL_0030
In-vivo Model 2 × 106 stably transfected HeLa cells were subcutaneously inoculated into the left flank of mice.
References
Ref 1 Downregulation of LncRNA DARS-AS1 Inhibits the Tumorigenesis of Cervical Cancer via Inhibition of IGF2BP3. Onco Targets Ther. 2021 Feb 25;14:1331-1340. doi: 10.2147/OTT.S274623. eCollection 2021.
Ref 2 Methyltransferase-like 3 induces the development of cervical cancer by enhancing insulin-like growth factor 2 mRNA-binding proteins 3-mediated apoptotic chromatin condensation inducer 1 mRNA stability. Bioengineered. 2022 Mar;13(3):7034-7048. doi: 10.1080/21655979.2022.2044261.