Downregulation of lncRNA AWPPH inhibits colon cancer cell proliferation by downregulating GLUT-1

lncRNA AWPPH 下调通过下调 GLUT-1 抑制结肠癌细胞增殖

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作者:Jie Bai, Jian Xu, Jian Zhao, Rui Zhang

Abstract

Long non-coding RNA (lncRNA) associated with poor prognosis of hepatocellular carcinoma (AWPPH) serves pivotal roles in bladder cancer and liver cancer; however, to the best of our knowledge, its functionality in colon cancer has not been characterized. The present study aimed to investigate the involvement of lncRNA AWPPH in colon cancer. Serum levels of lncRNA AWPPH and glucose transporter 1 (GLUT-1) in patients with early stage colon cancer and healthy controls were measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and ELISA. Correlation between lncRNA AWPPH and GLUT-1 expression was analyzed by Pearson's correlation coefficient. χ2 test was performed to investigate the associations between serum levels of lncRNA AWPPH and clinical data of patients with colon cancer. lncRNA AWPPH short hairpin RNA and GLUT-1 expression vectors were transfected into colon cancer cells, and the effects on lncRNA AWPPH, GLUT-1 and cell proliferation were detected by RT-qPCR, western blotting and Cell Counting Kit-8 assay. It was observed that serum levels of lncRNA AWPPH and GLUT-1 were significantly higher in patients with colon cancer patients compared with healthy controls. Serum levels of AWPPH and GLUT-1 were significantly positively correlated in patients with colon cancer. Serum levels of lncRNA AWPPH were associated with the tumor size. Furthermore, AWPPH-silencing significantly inhibited GLUT-1 expression and inhibited cancer cell proliferation. GLUT-1 overexpression promoted cancer cell proliferation and attenuated the inhibitory effects of AWPPH-silencing on cancer cell proliferation. However, GLUT-1 overexpression failed to significantly affect the expression of AWPPH. Therefore, it can be concluded that a downregulation of lncRNA AWPPH may inhibit colon cancer cell proliferation by downregulating GLUT-1.

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