Cancer Management and Research (Mar 2020)
LncRNA-SNHG16 Silencing Inhibits Prostate Carcinoma Cell Growth, Downregulate GLUT1 Expression and Reduce Glucose Uptake
Abstract
Mingfeng Shao, Ziqiang Yu, Jianan Zou Department of Urology, The First Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei City, Anhui Province 230031, People’s Republic of ChinaCorrespondence: Jianan ZouDepartment of Urology, The First Affiliated Hospital of Anhui University of Traditional Chinese Medicine, No. 117, Meishan Road, Hefei City, Anhui Province 230031, People’s Republic of ChinaTel +86 551-62850073Email [email protected]: lncRNA-SNHG16 was identified as an oncogene in many cancers, but its involvement in prostate carcinoma is unknown.Material and Method: Expression of lncRNA-SNHG16 and glucose transporter 1 (GLUT-1) in 52 prostate carcinoma tissues and 36 normal prostate tissues was analyzed by RT-qPCR. Transfections were performed to analyze gene interactions. Cell proliferation was analyzed by cell proliferation assay.Results: Overexpression of lncRNA-SNHG16 effectively distinguished prostate carcinoma patients from normal ones. Expression levels of lncRNA-SNHG16 and GLUT-1 mRNA were significantly and positively correlated across prostate carcinoma tissues. In vitro cancer cell experiments revealed that lncRNA-SNHG16 siRNA silencing downregulated the expressions of GLUT-1 and reduced glucose uptake. lncRNA-SNHG16 siRNA silencing also significantly inhibited prostate carcinoma cell proliferation. However, lncRNA-SNHG16 siRNA silencing did not affect the normal prostate.Conclusion: In conclusion, lncRNA-SNHG16 might be a possible treatment target for prostate cancer.Keywords: prostate carcinoma, SNHG16, glucose transporter 1
