Downregulation of USP18 inhibits growth and induces apoptosis in hepatitis B virus-related hepatocellular carcinoma cells by suppressing BCL2L1

Publication date: Available online 12 July 2017
Source:Experimental Cell Research
Author(s): Jing Cai, Tiande Liu, Xiaoliu Jiang, Changkuo Guo, Anwen Liu, Xinlan Xiao
Ubiquitin-specific peptidase 18 (USP18) is closely related with hepatitis B virus (HBV), which has been involved in tumourigenesis. However, there has been little research into the role of USP18 on the progression of hepatocellular carcinoma (HCC), especially in HBV-related HCC. In present study, we found that USP18 expression was aberrantly elevated in HCC tissues than adjacent non-tumour tissues. Importantly, USP18 expression was higher in HBV-related HCC cell lines (HepG2.2.15 and Hep3B) than HBV-unrelated HCC cell lines. Furthermore, knockdown of USP18 significantly suppressed tumor cell proliferation in vitro and tumor growth in vivo, whereas overexpression of USP18 promoted HCC cells growth. Moreover, our experimental data revealed that USP18 silencing obviously blocked cell cycle at G1 phase and increased cell apoptosis. Finally, BCL2L1, a member of BCL2 family protein, was identified as a downstream gene of USP18. Mechanistically, we found that USP18 directly bind to BCL2L1 and positively regulated its expression in HCC cells. Overall, our results suggested that USP18 has a crucial role in regulating diverse aspects of the pathogenesis of HCC, indicating that it might be a potential therapeutic target.



from # All Medicine by Alexandros G. Sfakianakis via Alexandros G.Sfakianakis on Inoreader http://ift.tt/2sSn5ba
via IFTTT