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MicroRNA-135a expression is upregulated in hepatocellular carcinoma and targets long non-coding RNA TONSL-AS1 to suppress cell proliferation

Authors
  • Deng, Xuesong
  • Cheng, Jun
  • Zhan, Naiyang
  • Chen, Jianwei
  • Zhan, Yongqiang
  • Ni, Yong
  • Liao, Caixian
Type
Published Article
Journal
Oncology Letters
Publisher
Spandidos Publications
Publication Date
Sep 24, 2021
Volume
22
Issue
5
Identifiers
DOI: 10.3892/ol.2021.13069
PMCID: PMC8488329
Source
PubMed Central
Keywords
Disciplines
  • Articles
License
Unknown

Abstract

Dysregulation of long non-coding RNAs (lncRNAs) results in development of human diseases, including hepatocellular carcinoma (HCC). lncRNA TONSL-AS1 has been reported to act as a tumor suppressor in gastric cancer. The present study aimed to investigate the role of TONSL-AS1 in hepatocellular carcinoma (HCC). Reverse transcription-quantitative PCR analysis was performed to detect the expression levels of TONSL-AS1 and microRNA (miRNA/miR)-135a in HCC tissues and paired adjacent normal tissues. A 5-year follow-up study was performed to determine the prognostic value of TONSL-AS1 in HCC. The association between miR-135a and TONSL-AS1 was assessed via overexpression experiments. The Cell Counting Kit-8 assay was performed to assess cell proliferation. The results demonstrated that TONSL-AS1 expression was downregulated in HCC tissues, which was associated with a lower survival rate in patients with HCC. TONSL-AS1 and miR-135a were predicted to interact with each other, whereby overexpression of miR-135a downregulated TONSL-AS1 expression. The results demonstrated that TONSL-AS1 and miR-135a were inversely correlated with each other. Notably, overexpression of TONSL-AS1 inhibited HCC cell proliferation, while overexpression of miR-135a promoted HCC cell proliferation and decreased the effect of overexpression of TONSL-AS1 on cell proliferation. Taken together, the results of the present study suggest that miR-135a expression is upregulated in HCC and targets lncRNA TONSL-AS1 to suppress cell proliferation.

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