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LncRNA-SNHG16 沉默可抑制前列腺癌细胞的生长、下调 GLUT1 表达并减少葡萄糖摄取
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
DOI https://doi.org/10.2147/CMAR.S231370
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 3
Editor who approved publication: Dr Eileen O'Reilly
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
