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MAP30, a type Ⅰ ribosome-inactivating protein, inhibits hepatocellular carcinoma by inducing apoptosis through
1The Second Affiliated Hospital of Chengdu Medical College, China National Nuclear Corporation 416 Hospital, Chengdu, Sichuan, China.
Background:
We have purified Momordica anti-HIV protein of 30 kDa (MAP30), a type I ribosome-inactivating protein from Momordica charantia L. with approximately 30 kDa, which inhibited protein synthesis through N-glycosylase activity and exhibited antiviral, antibacterial, antitumor and other biological activities. It is speculated that MAP30 may be a potential natural active agent for prevention and treatment of liver cancer. However, its effect on liver cancer and underlying mechanism are still unclear now. Therefore, the purpose of this manuscript was to explore the molecular mechanism of MAP30 on liver cancer.
Methods:
The cell counting kit-8 assay was used to detect the proliferation of SK-Hep-1 cells. The apoptosis, cell cycle, reactive oxygen species level and mitochondrial membrane potential of SK-Hep-1 cells were detected by flow cytometry. Protein levels were determined by Western blot.
Results:
It was confirmed that MAP30 can significantly inhibit the proliferation of SK-Hep-1 cells, arrest the cell cycle in G1 phase and induce apoptosis. Further studies on apoptosis-related proteins showed that the expression of caspase-3, caspase-9, poly (ADP-ribose) polymerase and B-cell lymphoma 2 proteins decreased synchronously in a time- and dose-dependent manner. In addition, MAP30-induced apoptosis of SK-Hep-1 cells was found to be closely related to the mitochondrial pathway through the increase of reactive oxygen species and the decrease of mitochondrial membrane potential.
Conclusion:
The manuscript indicated that MAP30 may be a potential antitumor drug which provided an experimental basis for further exploration of the mechanism of MAP30 prevention and treatment of liver cancer, and was expected to be applied in medicine and biotechnology.
Insights
Momordica anti-HIV protein of 30 kDa (MAP30) inhibits liver cancer cell proliferation and induces apoptosis. This study explores MAP30's molecular mechanism in liver cancer treatment, revealing its potential as an antitumor drug.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Momordica anti-HIV protein of 30 kDa (MAP30) is a ribosome-inactivating protein with known antiviral, antibacterial, and antitumor activities.
- MAP30's potential in liver cancer prevention and treatment is speculated but its mechanism remains unclear.
Purpose of the Study:
- To investigate the molecular mechanism of MAP30's effect on liver cancer cells.
- To explore MAP30 as a potential therapeutic agent for liver cancer.
Main Methods:
- Cell Counting Kit-8 assay for proliferation.
- Flow cytometry for apoptosis, cell cycle, reactive oxygen species (ROS), and mitochondrial membrane potential.
- Western blot for protein level analysis.
Main Results:
- MAP30 significantly inhibited SK-Hep-1 liver cancer cell proliferation.
- MAP30 induced G1 phase cell cycle arrest and apoptosis.
- Apoptosis involved the mitochondrial pathway, evidenced by increased ROS and decreased mitochondrial membrane potential, and affected key apoptosis-related proteins.
Conclusions:
- MAP30 demonstrates significant antitumor effects on liver cancer cells.
- MAP30's mechanism involves inducing apoptosis via the mitochondrial pathway.
- MAP30 shows promise as a potential antitumor drug for liver cancer treatment.
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