miR-31 Modulates Liver Cancer HepG2 Cell Apoptosis and Invasion via ROCK1/F-Actin Pathways
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Updated: Dec 27, 2025
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Published on: April 18, 2025
Xin Zhang1, Lan Xu1, Ting Yang1
1Department of Laboratory, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, People's Republic of China.
Purpose:
Liver cancer is one of the most common malignant tumor in the world. miR-31 is downregulated in liver cancer and associated with tumor growth and metastasis. However, the underlying mechanism remains unclear.
Methods:
Cellular apoptosis was detected via MTT, TUNEL assay, LDH release and Annexin V/PI flow-cytometry analysis. Cellular migration and invasion were measured by the Transwell chamber assay. Mitochondrial functions were evaluated via mitochondrial membrane potential JC-1 staining and mPTP opening assessment. The mitophagy activity was examined via Western blots.
Results:
In the present study, our results confirm that miR-31 promotes apoptosis and inhibits proliferation and metastasis in liver cancer HepG2 cells. In vitro, miR-31 promotes HepG2 cell apoptosis through the mitochondrial pathway as indicated by mitochondrial potential reduction, increased mPTP opening time, cty-c release and imbalance of pro- and anti-apoptotic proteins. Furthermore, miR-31 reduces the energy generation by inhibiting mitochondrial respiratory function. At last, it is demonstrated that miR-31 triggers the mitochondrial damage via ROCK1/F-actin pathway. Inhibiting the ROCK1/F-actin pathway abolishes the effects of miR-31 mimic on mitochondrial injury, apoptosis, proliferation arrest and migration inhibition.
Conclusion:
Our results reveal that miR-31 can inhibit HepG2 cell survival and metastasis by activating the ROCK1/F-actin pathway.
Insights
MicroRNA-31 (miR-31) inhibits liver cancer progression by inducing apoptosis and reducing metastasis in HepG2 cells. It achieves this by damaging mitochondria via the ROCK1/F-actin pathway, thus suppressing tumor growth.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Liver cancer is a prevalent malignancy globally.
- Downregulation of microRNA-31 (miR-31) is observed in liver cancer, correlating with tumor growth and metastasis.
- The precise molecular mechanisms underlying miR-31's role in liver cancer are not fully understood.
Purpose of the Study:
- To investigate the role of miR-31 in liver cancer cell apoptosis, proliferation, and metastasis.
- To elucidate the underlying molecular mechanisms, particularly focusing on mitochondrial function and the ROCK1/F-actin pathway.
Main Methods:
- Assessed apoptosis using MTT, TUNEL assay, LDH release, and Annexin V/PI flow cytometry.
- Measured cell migration and invasion with Transwell assays.
- Evaluated mitochondrial function via JC-1 staining, mPTP opening assessment, and Western blotting for mitophagy.
Main Results:
- miR-31 promotes apoptosis and inhibits proliferation and metastasis in HepG2 liver cancer cells.
- miR-31 induces apoptosis via the mitochondrial pathway, evidenced by reduced mitochondrial potential, increased mPTP opening, and altered apoptotic protein balance.
- miR-31 impairs mitochondrial respiratory function, reducing energy generation and triggering mitochondrial damage through the ROCK1/F-actin pathway.
Conclusions:
- miR-31 inhibits HepG2 cell survival and metastasis.
- Activation of the ROCK1/F-actin pathway by miR-31 is crucial for its tumor-suppressive effects.
- Targeting the ROCK1/F-actin pathway represents a potential therapeutic strategy for liver cancer.
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