Silencing of karyopherin α2 inhibits cell growth and survival in human hepatocellular carcinoma
Metrics: PDF 736 views | HTML 1775 views | ?
Yunfeng Yang1,2, Jian Guo3, Yuxia Hao2, Fuhua Wang4, Fengxia Li2, Shaomin Shuang1, Junping Wang2
1College of Chemistry and Chemical Engineering, Shanxi University, Taiyuan, 030006, Shanxi, China
2Department of Gastroenterology, Shanxi Provincial People’s Hospital, Taiyuan, 030012, Shanxi, China
3Department of General Surgery, Shanxi Provincial People’s Hospital, Taiyuan, 030012, Shanxi, China
4Department of Molecular Biology, Shanxi Cancer Hospital and Institute, Taiyuan, 030013, Shanxi, China
Shaomin Shuang, email: firstname.lastname@example.org
Junping Wang, email: email@example.com
Keywords: hepatocellular carcinoma, KPNA2, tumorigenesis, microarray, gene-interaction network
Received: September 09, 2016 Accepted: March 20, 2017 Published: March 31, 2017
Karyopherin α2 (KPNA2), involved in nucleocytoplasmic transport, has been reported to be upregulated in hepatocellular carcinoma and considered as a biomarker for poor prognosis. However, comprehensive studies of KPNA2 functions in hepatocellular carcinogenesis are still lacking. Our study examine the roles and related molecular mechanisms of KPNA2 in hepatocellular carcinoma development. Results show that KPNA2 knockdown inhibited the proliferation and growth of hepatocellular carcinoma cells in vitro and in vivo. KPNA2 knockdown also inhibited colony formation ability, induced cell cycle arrest and cellular apoptosis in two hepatocellular carcinoma cell lines, HepG2 and SMMC-7721. Furthermore, gene expression microarray analysis in HepG2 cells with KPNA2 knockdown revealed that critical signaling pathways involved in cell proliferation and survival were deregulated. In conclusion, this study provided systematic evidence that KPNA2 was an essential factor promoting hepatocellular carcinoma and unraveled potential molecular pathways and networks underlying KPNA2-induced hepatocellular carcinogenesis.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.