4.5 Article

LncRNA-SNHG16 Silencing Inhibits Prostate Carcinoma Cell Growth, Downregulate GLUT1 Expression and Reduce Glucose Uptake

Journal

CANCER MANAGEMENT AND RESEARCH
Volume 12, Issue -, Pages 1751-1757

Publisher

DOVE MEDICAL PRESS LTD
DOI: 10.2147/CMAR.S231370

Keywords

prostate carcinoma; SNHG16; glucose transporter 1

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Funding

  1. Shandong Natural Science Foundation [ZR2016HL12]

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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.

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