USP36 Facilitates the Progression of Hepatocellular Carcinoma by Upregulating Myc

Abstract

Objective: Our study will explore the function and regulatory mechanism of USP36 in hepatocellular carcinoma (HCC). Methods: USP36-overexpressed and USP36-knockdown cells were established. The USP36 and Myc level were checked by Western blotting and the cell viability was checked by the MTT method. The apoptotic rate was checked by flow cytometry, while the migration was detected by the Transwell assay. A xenograft model was constructed in nude mice to explore the function of USP36 in HCC. USP36-overexpressed and USP-knockdown cells were constructed by transfecting pcDNA3.1-USP36 and siRNA-USP36 (si-USP36), respectively. Myc-overexpressed cells were constructed by transfecting pcDNA3.1-Myc. Results: Significantly declined cell viability, increased apoptotic rate, elevated number of migrated cells, downregulated Myc, and repressed tumor growth were observed in USP36-knockdown HepG2 and HUH7 cells, while opposite results were observed in USP36-overexpressed HepG2 and HUH7 cells. The expression level of Myc was positively regulated by USP36. However, the USP36 level was not regulated by Myc. Lastly, the declined cell viability, increased apoptotic rate, and elevated number of migrated cells in USP36-knockdown HepG2 cells were dramatically abrogated by the overexpression of Myc. Conclusion: USP36 facilitated the progression of hepatocellular carcinoma by upregulating Myc.