Mitochondrial transplantation therapy inhibits the proliferation of malignant hepatocellular carcinoma and its mechanism

Mitochondrial dysfunction plays a vital role in growth and malignancy of tumors. In recent scenarios, mito-chondrial transplantation therapy is considered as an effective method to remodel mitochondrial function in mitochondria-related diseases. However, the mechanism by which mitochondrial transplantation blocks tumor cell proliferation is still not determined. In addition, mitochondria are maternal inheritance in evolution, and mitochondria obtained from genders exhibit differences in mitochondrial activity. Therefore, the study indicates the inhibitory effect of mitochondria from different genders on hepatocellular carcinoma and explores the mo-lecular mechanism. The results reveal that the healthy mitochondria can retard the proliferation of the hepa-tocellular carcinoma cells in vitro and in vivo through arresting cell cycle and inducing apoptosis. The molecular mechanism suggests that mitochondrial transplantation therapy can decrease aerobic glycolysis, and down-regulate the expression of cycle-related proteins while up-regulate apoptosis-related proteins in tumor cells. In addition, the antitumor activity of mitochondria from female mice (F-Mito) is relatively higher than that of mitochondria from male mice (M-Mito), which would be related to the evidence that the F-Mito process higher activity than the M-Mito. This study clarifies the mechanism of exogenous mitochondria inhibiting the prolif-eration of hepatocellular carcinoma and contributes a new biotechnology for therapy of mitochondria-related diseases from different genders.

Automated summary

Mitochondrial dysfunction is closely related to tumor growth and malignancy, and mitochondrial transplantation therapy can improve the function of mitochondria-related diseases. The inhibitory mechanism of mitochondrial transplantation on tumor cell proliferation is still unknown. This study found that mitochondria from females have a stronger inhibitory effect on hepatocellular carcinoma, possibly due to their higher activity.