A new mechanism for mitochondrial autophagy to regulate the occurrence of liver cancer.

Primary liver cancer is a common primary malignancy that originates in the epithelial or interlocutoric tissue of the liver, and more than half of the world's new and dead liver cancer patients occur in China, but the mechanism of its development is not clear.
mitochondrial abnormality and mitochondrial metabolic disorders are closely related to the occurrence of liver cancer, while chronic inflammatory response is also an important factor to promote the occurrence of liver cancer.
mitochondrial autophagy is an important mechanism for selective removal of damaged mitochondria within cells, which is very important to maintain the quality of mitochondria, however, whether the abnormality of mitochondrial autophagy is involved in chronic inflammatory regulation and tumor occurrence is an urgent scientific problem to be solved.
researchers at the Institute of Zoology of the Chinese Academy of Sciences, Chen Wei, found that mitochondrial in vitro membrane protein FUNDC1 can mediate the removal of damaged mitochondria through autophagy, playing a key role in maintaining the steady state of the cell mitochondria.
in order to study the role of FUNDC1-mediated mitochondrial autophagy in the occurrence of liver cancer, the team first constructed the mice in which the liver specifically knocked out the FUNDC1 gene, and used diethhyaeamine (DEN) to induce the occurrence of primary liver cancer.
they found that mitochondrial autophagy receptor protein FUNDC1 promoted tumor sydctrice in the liver after specific knockout. Further research
further studies have shown that in liver cells, FUNDC1 deficiency causes damaged mitochondria to accumulate in the liver, and a large amount of mitochondrial DNA released from mitochondrial matrix to activate inflammatory small cells in the cytoplasm, over-activated inflammatory small cells produce a large number of inflammatory factors such as IL1, stimulate macrophage-induced cytofactors (TNF and IL6 etc.) storms to activate downstream signaling pathways such as JAK/STATand and the eventual proliferation of liver cancer.
mitochondrial autophagy can inhibit the activation of inflammatory cells and inhibit the development of liver cancer, provide new insights on the mechanism of cancer, and bring new possibilities for the diagnosis and treatment of liver cancer.
the results of the study were published in the journal Hepatology. Li Wenhui, a doctoral student at
, is the first author of the thesis, and Chen Wei is the communication author of the thesis.
the research was supported by the National Natural Science Foundation of China, the Ministry of Science and Technology of the People's Republic of China and the Beijing Natural Science Foundation.
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