The Institute of Biophysics has made progress in the research of Hippo signaling pathway and cancer and cell aging

October 17, 2020

The Hpo / MST-Yki / YAP pathway plays a very important role in regulating cell growth and organ size. YAP2 (Yes associated protein2), as the core protein of this pathway, is involved in tumor development. Yuan Qiang's research group of the Institute of Biophysics, Chinese Academy of Sciences has been concerned about and studying the molecular regulatory mechanism of YAP2 and its function in tumorigenesis. Recently, his research results were published in Oncogene and Cancer Research.

An article published online on Oncogene on April 1, 2013 reported the role of YAP2's new molecular regulatory mechanism in hepatocellular carcinoma cell proliferation and drug resistance. YAP2, as a proto-oncoprotein, has various post-translational modifications (phosphorylation and ubiquitination, etc.) to regulate its transcriptional activity and function. Research reveals YAP2's new post-translational modifications—acetylation and deacetylation, identifying SIRT1 as the main deacetylase of YAP2, enhancing the binding of YAP2 to the transcription factor TEAD4, promoting its transcriptional activity, and in ) Under treatment, YAP2 enters the nucleus and functions as a transcription factor, thereby enhancing the proliferation of liver cancer cells and resistance to anti-tumor drugs. Correspondingly, the protein level of SIRT1 in liver cancer specimens is significantly higher than that of normal tissues, and it is significantly positively correlated with the expression of downstream target gene CTGF of YAP2. These results provide a new basis for revealing the mechanism of liver cancer development and treatment of liver cancer.

Cell aging is an important mechanism for inhibiting tumorigenesis. Yuan Qiang's research team discovered that YAP2 functions as a new proto-oncoprotein—inhibit aging. The expression of YAP2 is decreased in IMR90, a normal human diploid cell that replicates. The interference of YAP2 directly induces cell senescence, which is dependent on TEAD and Rb / p16 / p53 pathways. The study found that CDK6 is a downstream target gene that mainly mediates YAP2 inhibition of aging and is regulated by the YAP / TEAD transcription complex. By overexpressing CDK6 in YAP2 interfered cells, it is possible to reverse the cell aging caused by the down-regulation of YAP2 protein. In addition to normal cells, the down-regulation of YAP2 protein can also significantly enhance the senescence of tumor cells induced by chemical drugs, indicating that YAP2 also has anti-aging functions in tumor cells, revealing a new mechanism of YAP2 promoting tumorigenesis and development. This result was published online at Cancer Research in April 2013.

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