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

Xiaoli Chen,Hui Wang,Lili Wang

doi:10.3892/ol.2019.10682

Xiaoli Chen, Hui Wang + Show 1 more

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https://doi.org/10.3892/ol.2019.10682

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Journal: Oncology letters	Publication Date: Jul 29, 2019
Citations: 8	License type: cc-by

Affiliation: Qingdao Eighth People's Hospital

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.

Highlights

Liver cancer is one of the most frequently diagnosed human malignancies and is one of the leading causes of cancer‐associated mortality worldwide [1]
LINC01638 long non‐coding RNA (lncRNA) and Glucose transporter 1 (GLUT1) mRNA are upregulated in tumor tissues compared with adjacent healthy tissues of patients with hepatocellular carcinoma (HCC)
Glucose uptake assay indicated that, compared with the control and the negative control groups, overexpression of LINC01638 lncRNA and GLUT1 led to a significant increase in glucose uptake (Fig. 3A), while LINC01638 lncRNA and GLUT1‐knockdown led to a significant inhibition in glucose uptake (Fig. 3B) in SNU‐398 and SNU‐182 cells (P

Summary

Introduction

Liver cancer is one of the most frequently diagnosed human malignancies and is one of the leading causes of cancer‐associated mortality worldwide [1]. The incidence of liver in the majority of developed countries is increasing [2]. Cancer cells are characterized by accelerated energy metabolism compared with normal cells [7]. A growing body of literatures has indicated that GLUT1 contributes to the development of different types of cancer, partially through the interactions with long non‐coding RNAs (lncRNAs) [10,11], which are a subgroup of non‐coding RNAs with critical roles in cancer biology [12]. It is has been previously reported that long intergenic non‐protein coding RNA 1638 (LINC01638) promotes breast cancer [13], while its roles in other types of cancers remain unclear. The present study indicated that LINC01638 lncRNA promoted cancer cell proliferation in hepatocellular carcinoma (HCC), a major type of liver cancer, potentially by increasing cancer cell glucose uptake and promoting GLUT1 expression

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