Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05448
[1]
m6A modification KCNMB2-AS1 KCNMB2-AS1 IGF2BP3 : m6A sites Direct Enhancement Non-coding RNA KCNMB2-AS1 miR-130b-5p  lncRNA       miRNA   circRNA
m6A Modification:
m6A Regulator Insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) READER
m6A Target KCNMB2 antisense RNA 1 (KCNMB2-AS1)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator KCNMB2 antisense RNA 1 (KCNMB2-AS1) LncRNA View Details
Regulated Target hsa-miR-130b-5p View Details
Crosstalk Relationship m6A  →  ncRNA Enhancement
Crosstalk Mechanism m6A regulators directly modulate the functionality of ncRNAs through specific targeting ncRNA
Crosstalk Summary KCNMB2 antisense RNA 1 (KCNMB2-AS1) and IGF2BP3 formed a positive regulatory circuit that enlarged the tumorigenic effect of KCNMB2-AS1 in cervical cancer. KCNMB2-AS1 was predominantly located in the cytoplasm and served as a competing endogenous RNA to abundantly sponge hsa-miR-130b-5p and miR-4294, resulting in the upregulation of IGF2BP3, a well-documented oncogene in CC.
Responsed Disease Cervical cancer ICD-11: 2C77
Pathway Response Apoptosis hsa04210
Cell Process Cell proliferation
Cell apoptosis
In-vitro Model
SiHa Cervical squamous cell carcinoma Homo sapiens CVCL_0032
HeLa Endocervical adenocarcinoma Homo sapiens CVCL_0030
In-vivo Model A total of 1 × 107 control or KCNMB2-AS1-depleted SiHa cells were resuspended in 0.1 ml phosphate-buffered saline and inoculated into the armpit of 5-week-old male BALB/c nude mice.
References
Ref 1 Long Noncoding RNA KCNMB2-AS1 Stabilized by N(6)-Methyladenosine Modification Promotes Cervical Cancer Growth Through Acting as a Competing Endogenous RNA. Cell Transplant. 2020 Jan-Dec;29:963689720964382. doi: 10.1177/0963689720964382.