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Updated: Dec 26, 2025
08:56
A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues
Published on: December 5, 2016
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SIRT1 Regulates N6 -Methyladenosine RNA Modification in Hepatocarcinogenesis by Inducing RANBP2-Dependent FTO
Xiaoming Liu1,2, Jianye Liu3, Wen Xiao4
1Department of Oncology, Third Xiangya Hospital of Central South University, Changsha, China.
Hepatology (Baltimore, Md.)
|March 11, 2020
Summary
Silent information regulator 1 (SIRT1) promotes hepatocellular carcinoma (HCC) by destabilizing the m6 A demethylase FTO. This mechanism drives HCC tumorigenesis, revealing SIRT1 as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Hepatocellular carcinoma (HCC) exhibits high malignancy.
- Silent information regulator 1 (SIRT1) is linked to HCC malignancy and metastasis.
- The role of SIRT1 in regulating N6 -methyladenosine (m6 A) modification in hepatocarcinogenesis is unclear.
Purpose of the Study:
- To elucidate the mechanism by which SIRT1 regulates m6 A modification in HCC.
- To investigate the role of SIRT1 in HCC tumorigenesis.
Main Methods:
- Investigated the interaction between SIRT1 and FTO (an m6 A demethylase).
- Examined the role of RANBP2 in FTO SUMOylation and degradation.
- Identified downstream targets of FTO, including GNAO1.
Main Results:
- SIRT1 down-regulates FTO expression, promoting HCC.
- SIRT1 activates RANBP2, leading to FTO SUMOylation and degradation.
- FTO depletion by SIRT1 results in increased m6 A modification of GNAO1, a tumor suppressor, and decreased GNAO1 mRNA expression.
Conclusions:
- SIRT1 destabilizes FTO, influencing m6 A modification of downstream targets and mRNA expression in HCC.
- This mechanism highlights SIRT1 as a potential therapeutic target for HCC treatment.
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