LINC01638 lncRNA promotes cancer cell proliferation in hepatocellular carcinoma by increasing cancer cell glucose uptake

Chen,Xiaoli; Wang,Lili; Wang,Hui

doi:10.3892/ol.2019.10682

LINC01638 lncRNA promotes cancer cell proliferation in hepatocellular carcinoma by increasing cancer cell glucose uptake

Authors:
- Xiaoli Chen
- Lili Wang
- Hui Wang
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Affiliations: Ten Areas of Liver Disease, Sixth People's Hospital of Qingdao, Qingdao, Shandong 266000, P.R. China
Published online on: July 29, 2019 https://doi.org/10.3892/ol.2019.10682
Pages: 3811-3816

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Abstract

The aim of the present study was to examine the function of long intergenic non‑protein coding RNA 1638 (LINC01638) long non‑coding RNA (lncRNA) in hepatocellular carcinoma (HCC). In the present study, gene expression was analyzed using qPCR and western blotting. Glucose uptake was analyzed using a glucose uptake assay and cell proliferation was analyzed using a cell counting kit‑8 assay. LINC01638 lncRNA and glucose transporter 1 (GLUT1) were upregulated in tumor tissues compared with adjacent healthy tissues of patients with HCC. Expression levels of LINC01638 lncRNA and GLUT1 were positively correlated only in tumor tissues; however, there was no correlation in adjacent healthy tissues. Overexpression of LINC01638 lncRNA and GLUT1 promoted glucose uptake, while LINC01638 lncRNA and GLUT1‑knockdown led to inhibited glucose uptake of cells of HCC cell lines. Overexpression of LINC01638 lncRNA mediated the upregulation of GLUT1 expression and accelerated cell proliferation. GLUT1 overexpression failed to significantly affect LINC01638 lncRNA expression, however also promoted cancer cell proliferation. In addition, GLUT1‑knockdown attenuated the effects of LINC01638 overexpression on cancer cell proliferation. Therefore, LINC01638 lncRNA promoted cancer cell proliferation in HCC, potentially by increasing cancer cell glucose uptake.

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