m6A Target Gene Information
General Information of the m6A Target Gene (ID: M6ATAR00110)
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
MIR1305
can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
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Methyltransferase-like 3 (METTL3) [WRITER]
In total 1 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
Response Summary | circ-ARL3 is a critical regulator in HBV-related HCC, targeting the axis of circ-ARL3/microRNA 1305 (MIR1305) can be a promising treatment for HBV+ HCC patients. HBx protein upregulated N6 -methyladenosine (m6A) methyltransferases METTL3 expression, increasing the m6A modification of circ-ARL3; then, m6A reader YTHDC1 bound to m6 A-modified of circ-ARL3 and favored its reverse splicing and biogenesis. Furthermore, circ-ARL3 was able to sponge miR-1305, antagonizing the inhibitory effects of miR-1305 on a cohort of target oncogenes, thereby promoting HBV+ HCC progression. | |||
Target Regulation | Up regulation | |||
Responsed Disease | Hepatocellular carcinoma | ICD-11: 2C12.02 | ||
Cell Process | Reverse splicing and biogenesis | |||
In-vitro Model | Hep-G2 | Hepatoblastoma | Homo sapiens | CVCL_0027 |
In-vivo Model | Mice were randomly divided into three groups, and subcutaneously injected with control, circ-ARL3-silenced and circ-ARL3&miR-1305-silenced HepG2.2.15 cells. | |||
Liver cancer [ICD-11: 2C12]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | circ-ARL3 is a critical regulator in HBV-related HCC, targeting the axis of circ-ARL3/microRNA 1305 (MIR1305) can be a promising treatment for HBV+ HCC patients. HBx protein upregulated N6 -methyladenosine (m6A) methyltransferases METTL3 expression, increasing the m6A modification of circ-ARL3; then, m6A reader YTHDC1 bound to m6 A-modified of circ-ARL3 and favored its reverse splicing and biogenesis. Furthermore, circ-ARL3 was able to sponge miR-1305, antagonizing the inhibitory effects of miR-1305 on a cohort of target oncogenes, thereby promoting HBV+ HCC progression. | |||
Responsed Disease | Hepatocellular carcinoma [ICD-11: 2C12.02] | |||
Target Regulator | Methyltransferase-like 3 (METTL3) | WRITER | ||
Target Regulation | Up regulation | |||
Cell Process | Reverse splicing and biogenesis | |||
In-vitro Model | Hep-G2 | Hepatoblastoma | Homo sapiens | CVCL_0027 |
In-vivo Model | Mice were randomly divided into three groups, and subcutaneously injected with control, circ-ARL3-silenced and circ-ARL3&miR-1305-silenced HepG2.2.15 cells. | |||