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Updated: Sep 6, 2025

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
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Published on: September 12, 2019

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Research on Mfn2 Gene Expression in Hepatocellular Carcinoma and its Antitumor Mechanism

Yushuang Huang, Wei Gao, Yingde Wang

    Alternative Therapies in Health and Medicine
    |June 25, 2022
    PubMed
    Abstract

    Insights

    Mitochondشاف-2 (Mfn2) gene expression is reduced in hepatocellular carcinoma (HCC). Overexpressing Mfn2 inhibits HCC cell activity and induces autophagy, suggesting a potential anticancer effect.

    Area of Science:

    • Oncology
    • Molecular Biology
    • Cell Biology

    Background:

    • Hepatocellular carcinoma (HCC) is a prevalent cancer with complex molecular underpinnings.
    • Mitochondrial dynamics protein 2 (Mfn2) plays a role in cellular processes, but its specific function in HCC is not fully understood.

    Purpose of the Study:

    • To investigate the expression levels of Mfn2 in HCC tissues and adjacent normal tissues.
    • To analyze the anticancer effects of Mfn2 in HCC by examining its impact on cell activity and autophagy.

    Main Methods:

    • Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting were used to detect gene and protein expression.
    • The HepG2 human HCC cell line was utilized for in vitro experiments.
    • Mfn2 overexpression was achieved through plasmid transfection.
    • Cell Counting Kit-8 (CCK-8) assay assessed cell activity.

    Main Results:

    • Mfn2, GLS1, Beclin1, and lc3b mRNA levels were lower in HCC tissues compared to adjacent normal tissues.
    • Mfn2, Beclin1, and lc3b expression decreased in HCC cells, while GLS1 expression increased.
    • Mfn2 overexpression inhibited HepG2 cell activity and GLS1 expression.
    • Mfn2 overexpression induced autophagy by upregulating Beclin-1 and lc3b.

    Conclusions:

    • Mfn2 expression is downregulated in HCC.
    • Mfn2 overexpression exhibits anticancer properties by inhibiting HCC cell activity and promoting autophagy.
    • Mfn2 may represent a potential therapeutic target for HCC, though further mechanistic studies are warranted.

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