Medicine · 2026
MAP30, a type Ⅰ ribosome-inactivating protein, inhibits hepatocellular carcinoma by inducing apoptosis through mitochondria.
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Yang Di, Peng Di, Jia Di, Zhou Yiping, Li Houke, Jiang Zongxing, Meng Yao
Аннотация
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.
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.