Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05917
[1]
Non-coding RNA piRNA-17458 WTAP  lncRNA       miRNA   circRNA Direct Enhancement m6A modification m6A Target m6A Target WTAP Methylation : m6A sites
m6A Modification:
m6A Regulator Wilms tumor 1-associating protein (WTAP) WRITER
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator piR-17458 piRNA View Details
Regulated Target Pre-mRNA-splicing regulator WTAP (WTAP) View Details
Crosstalk Relationship ncRNA  →  m6A Enhancement
Crosstalk Mechanism ncRNAs directly impacts m6A modification through modulating the expression level of m6A regulator
Crosstalk Summary piR-17458 promotes tumorigenesis of CC in a WTAP-mediated m6A methylation manner.
Responsed Disease Cervical cancer ICD-11: 2C77
Cell Process Cell migration, Cell invasion
Cell proliferation
In-vitro Model
Ca Ski Cervical squamous cell carcinoma Homo sapiens CVCL_1100
SiHa Cervical squamous cell carcinoma Homo sapiens CVCL_0032
End1/E6E7 Normal Homo sapiens CVCL_3684
HUCECs (Human Uterine Cervical Epithelial Cells)
In-vivo Model A total of 5×106 Caski cells were subcutaneously injected into the left inguen of mice. When tumors were ~50 mm3±10% (day16). The mice were randomly divided into 4 groups and received piRNA-17458 mimic or piRNA-17458 inhibitor by intratumor injection for every 4 days for a total of five injections. On the 36th day, the tumor weight and lymph node metastasis of the nude mice were assessed after mice were euthanized.
References
Ref 1 PIWI-interacting RNA-17458 is oncogenic and a potential therapeutic target in cervical cancer. J Cancer. 2023 Jun 4;14(9):1648-1659. doi: 10.7150/jca.83446. eCollection 2023.