Tumor mitochondria alter their functions to reprogram cell metabolism and then allow tumor cells to rapidly proliferate in the hypoxic and acidic microenvironment. However, roles of normal mitochondria played in tumor progression are still unclear. Here we investigate the normal mitochondrial effect on abnormal metabolism of tumors, and to clarify why the mitochondria have to undergo functional changes in the tumor growth. The mitochondria isolated from healthy mouse livers were intravenously injected into melanoma model mice with lung metastasis, then the tumor growth, animal survival and associated metabolic changes were studied. The results reveal that the mitochondria significantly retard tumor growth and increase survival days of animals. The anti-tumor effect of the mitochondria is related to interfering the tumor cell metabolisms, such as reducing glycolysis and producing an oxidative intracellular environment, all of which are not suitable for tumor cell proliferation. In addition, the mitochondria increases cell apoptosis, necrosis, and mitophagy. These effects are more efficient with the mitochondria isolated from young mouse livers than those from aged mice. Our study not only provides a valuable approach to invest mitochondrial function associated with tumor growth but also offer new insight into tumor therapy through interfering the tumor cell metabolism by healthy mitochondria.
Keywords: bioenergy; isolated mitochondria; melanoma; redox.
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