CMTM6 promotes hepatocellular carcinoma progression through stabilizing β-catenin.

Cancer Lett

Department of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, NHC Key Laboratory of Medical Immunology (Peking University), Beijing, China; Peking University Center for Human Disease Genomics, Beijing, China, Beijing, China. Electronic address:

Published: February 2024


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Article Abstract

CMTM6, a regulator of PD-L1 stability, has been implicated in the development of various cancers. However, the expression and role of CMTM6 in hepatocellular carcinoma (HCC) remains controversial. Our study revealed a negative correlation between CMTM6 expression and HCC prognosis through bioinformatics analysis and immunofluorescence staining. CMTM6 expression was also positively associated with alpha-fetoprotein (AFP) levels, supporting its potential as a prognostic marker for HCC. Using Cmtm6 knockout mice, we found that Cmtm6 deficiency inhibited HCC formation and cell proliferation in primary liver cancer models induced by DEN and DEN/CCl. In HCC cell lines, CMTM6 promoted cell proliferation and interacted with β-catenin, stabilizing it by preventing ubiquitination. In conclusion, our study suggested that CMTM6 upregulation promotes HCC cell proliferation through the β-catenin pathway, making it a potential therapeutic target for HCC treatment.

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http://dx.doi.org/10.1016/j.canlet.2023.216585DOI Listing

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