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Updated: Sep 2, 2025
06:07
Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
Published on: August 5, 2022
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SETD3 Methyltransferase Regulates PLK1 Expression to Promote In Situ Hepatic Carcinogenesis
Meng Cheng1, Qingmiao Yang2, Yafei Liu1
1Hubei Key Laboratory of Cell Homeostasis, RNA Institute, College of Life Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, China.
Frontiers in Oncology
|August 1, 2022
Summary
Elevated SETD3 promotes hepatocellular carcinoma (HCC) by increasing PLK1 expression. Targeting SETD3 with PLK1 inhibition offers a potential new strategy for HCC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Hepatology
Background:
- Hepatocellular carcinoma (HCC) chemoresistance remains a significant clinical challenge.
- Upregulated SET domain containing 3 (SETD3) levels are correlated with HCC.
- This study investigates the mechanism by which SETD3 promotes liver carcinogenesis.
Purpose of the Study:
- To elucidate the mechanism of SETD3-mediated promotion of liver carcinogenesis.
- To explore the relationship between SETD3 and Polo-like kinase 1 (PLK1) in HCC.
- To identify potential therapeutic targets for HCC treatment.
Main Methods:
- RNA-Sequencing to identify SETD3 regulatory targets.
- In vitro assays (cell proliferation, migration) to assess oncogenic roles.
- Western blotting, immunohistochemistry, and biochemical assays to evaluate protein expression and pathological indices.
- Luciferase reporter and chromatin immunoprecipitation assays to determine molecular mechanisms.
Main Results:
- SETD3 regulates gene expression related to cell division, proliferation, and cell cycle in HCC cells.
- SETD3 upregulation correlates with elevated PLK1 levels in HCC cells and tissues.
- SETD3 overexpression enhances tumor cell proliferation and migration; PLK1 inhibition mitigates these effects.
- SETD3 promotes HCC in vivo, and PLK1 knockdown reduces SETD3-induced tumorigenesis.
- SETD3 directly facilitates PLK1 transcription by binding to the PLK1 promoter.
Conclusions:
- Elevated SETD3 promotes HCC by enhancing PLK1 expression.
- SETD3 may serve as a potential therapeutic target in combination with PLK1 inhibition for HCC treatment.
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