m6A-centered Crosstalk Information
Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
| Crosstalk ID |
M6ACROT05050
|
[1] | |||
Non-coding RNA
GAS5-AS1
ALKBH5
lncRNA miRNA circRNA
Indirect
Inhibition
m6A modification
GAS5
GAS5
YTHDF2
 : m6A sites
|
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| m6A Modification: | |||||
|---|---|---|---|---|---|
| m6A Regulator | YTH domain-containing family protein 2 (YTHDF2) | READER | |||
| m6A Target | Growth arrest specific 5 (GAS5) | ||||
| Epigenetic Regulation that have Cross-talk with This m6A Modification: | |||||
| Epigenetic Regulation Type | Non-coding RNA (ncRNA) | ||||
| Epigenetic Regulator | GAS5 antisense RNA 1 (GAS5-AS1) | LncRNA | View Details | ||
| Regulated Target | RNA demethylase ALKBH5 (ALKBH5) | View Details | |||
| Crosstalk Relationship | ncRNA → m6A | Inhibition | |||
| Crosstalk Mechanism | ncRNAs indirectly impacts m6A modification through downstream signaling pathways | ||||
| Crosstalk Summary | GAS5-AS1 interacted with the tumor suppressor Growth arrest specific 5 (GAS5), and increased its stability by interacting with RNA demethylase RNA demethylase ALKBH5 (ALKBH5) and decreasing GAS5 N6-methyladenosine (m6A) modification. Moreover, it was shown that m6A-mediated GAS5 RNA degradation relied on the m6A reader protein YTHDF2-dependent pathway. Our findings reveal an important mechanism of epigenetic alteration in CC carcinogenesis and metastasis. | ||||
| Responsed Disease | Cervical cancer | ICD-11: 2C77 | |||
| Cell Process | Cell proliferation and metastasis | ||||
In-vitro Model |
Ca Ski | Cervical squamous cell carcinoma | Homo sapiens | CVCL_1100 | |
| SiHa | Cervical squamous cell carcinoma | Homo sapiens | CVCL_0032 | ||
| C-33 A | Cervical squamous cell carcinoma | Homo sapiens | CVCL_1094 | ||
| HeLa | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | ||
| In-vivo Model | 200 μ L PBS containing 1× 107 cells of stable cells were subcutaneously injected into male BALB/c athymic nude mice (6-week old, 18-20 g). | ||||