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miR-31 Modulates Liver Cancer HepG2 Cell Apoptosis and Invasion via ROCK1/F-Actin Pathways
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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