ZNF382 inhibits hepatocellular carcinoma (HCC) cell proliferation and motility and induces apoptosis by up-regulating SOX11

Abstract

Background and Objective: To detect the mRNA and protein levels of Zinc-finger protein382 (ZNF382) in human hepatocellular carcinoma (HCC) tissues and cell lines and investigate its effects on the cellular processes of HCC cells in vitro. Methods: Quantitative PCR and Immunoblot assays were respectively conducted to detect the alteration of ZNF382 mRNA and protein levels in HCC human tissues and cell lines. MTT, FCM, wound closure, and transwell assays were performed to detect the effects of ZNF382 on HCC cell proliferation, apoptosis, and motility of HCC cells in vitro. Immunoblot assays were then performed to detect the effects of ZNF382 on the expression of Signal Transducer and Activator of Transcription 3 (STAT3) and SOX11 in HCC cells, and the rescue assays were conducted to confirm the conclusion. Results: We found ZNF382 was low expression in human HCC tissues and cell lines. ZNF382 suppressed the proliferation and stimulated the apoptosis of HCC cells. Additionally, ZNF382 inhibited the motility of HCC cells in vitro. Mechanically, ZNF382 mediated STAT3/SOX11, and therefore affected the proliferation, apoptosis, and motility of HCC cells. Conclusion: We showed the abnormal low expression of ZNF382 in human HCC tissues and cell lines, and confirmed the effects of ZNF382 on HCC cellular processes. We thought ZNF382 was a tumor suppressor in HCC.

Keywords

• zinc-finger protein382 (znf382)
• hepatocellular carcinoma (hcc)
• signal transducer and activator of transcription 3 (stat3)
• sox11
• proliferation
• apoptosis