LncRNA-SNHG16 Silencing Inhibits Prostate Carcinoma Cell Growth, Downregulate GLUT1 Expression and Reduce Glucose Uptake
Authors Shao M, Yu Z, Zou J
Received 17 September 2019
Accepted for publication 10 January 2020
Published 9 March 2020 Volume 2020:12 Pages 1751—1757
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Eileen O'Reilly
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 China
Correspondence: Jianan Zou
Department 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 China
Tel +86 551-62850073
Background: 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
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