Íò²©Ë®¾§¹¬

LI Qing ^1,2¢Ú , XU Qi ^1,2 ,ZHANG Chong ^1,2¢Û

(1. Guangxi Key Laboratory of Molecular Medicine in Liver Injury and Repair, the Affiliated Hospital of Guilin Medical University, Guilin 541001; 2. Guangxi Health Commission Key Laboratory of Basic Research in Sphingolipid Metabolism Related Diseases, the Affiliated Hospital of Guilin Medical University, Guilin 541001, China)

Abstract Objective: To investigate the role and mechanism of UFC1 in liver cancer progression.Methods: TCGA database was used to analyze the expression of UFC1 in liver cancer tissues and to detect the relationship between its expression and the prognosis of HCC patients. Hepa1-6 murine cells were constructed by infection with lentivirus to form a stable knockdown cell line of UFC1. Colony formation experiment was used to detect the proliferation of cells. Silencing the expression of UFC1 by transiently transfecting cells with siRNA, the mRNA and protein expression levels of YAP and its downstream cyclin were detected by real-time fluorescent quantitative PCR (RT-qPCR) and Western blot, respectively. Results: The database analysis results showed that UFC1 was highly expressed in liver cancer tissues and was associated with poor prognosis. After UFC1 knockdown, the proliferation of hepatoma cells was decreased, the expression of YAP protein was down-regulated, and the expression of CCNA2 was significantly reduced. Conclusion: UFC1 is highly expressed in liver cancer, indicating poor prognosis ofpatients. UFC1 silencing can down-regulate the expression of YAP and its downstream CCNA2, and inhibit the proliferation of mouse liver cancer cells. It suggests that UFC1 may be a potential target for the treatment of liver cancer.

Keywords: liver cancer; UFC1; YAP; CCNA2

DOI:10.19296/ j.cnki.1008-2409.2023-01-004

PDF download:click to download