Zunli Yi,Xiaoguang Guo,Xianxue Jiang,Fengmei Luo. Effects of long non-coding RNA GAS5 on proliferation and apoptosis of hepatocellular carcinoma cells through miR-26a-5p action. Oncol Transl Med, 2022, 8: 126-134.
Effects of long non-coding RNA GAS5 on proliferation and apoptosis of hepatocellular carcinoma cells through miR-26a-5p action
Received:July 07, 2021  Revised:June 29, 2022
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KeyWord:lncRNA GAS5; miR-26a-5p; hepatocellular carcinoma (HCC); cell proliferation; cell cycle; apoptosis
Author NameAffiliationE-mail
Zunli Yi Pathology Department, Yuechi People''s Hospital zhuichengkong2351@163.com 
Xiaoguang Guo Pathology Department, Nanchong Central Hospital  
Xianxue Jiang The First Department of General Surgery, Yuechi People''s Hospital  
Fengmei Luo The Second Department of General Surgery, Yuechi People''s Hospital  
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Abstract:
      Objective Long non-coding RNAs (lncRNAs) regulate tumor development and progression by promoting tumor proliferation, invasion, and metastasis. The aim of the study was to investigate the effects of lncRNA growth arrest-special 5 (GAS5) on proliferation and apoptosis of hepatocellular carcinoma (HCC) cells through miR-26a-5p action. Methods Expression levels of GAS5 were detected in cancerous and paracancerous tissue of 80 HCC patients by RT-qPCR. The starBase tool predicted that GAS5 had binding sites for the miRNA miR-26a-5p, which was also highly expressed in HCC tissue. The relationship between GAS5 and miR-26a-5p was confirmed using a luciferase reporter assay. The role of these lncRNAs was further explored by transfecting plasmids into SMMC-7721 cells and classifying the cells as follows: NC group, GAS5 group, anti-miR- 26a-5p group, and GAS5 + miR-26a-5p group. Cell proliferation, cell cycle, and apoptosis were detected in each group. The relationship between miR-26a-5p and phosphatase and tensin homolog deleted on chromosome 10 (PTEN) was analyzed by TargetScan database prediction and luciferase reporter assay. Western blotting was used to quantify PTEN, phosphatidylinositol 3-kinase (PI3K), phosphorylated protein kinase B (p-Akt), cyclin D1, and human P27 protein (P27). Results GAS5 was downregulated, while miR-26a-5p was upregulated in HCC tissue compared to in paracancerous tissue. High GAS5 levels and low miR-26a-5p levels inhibited cell proliferation, increased the number of G0/G1 phase cells, promoted cell apoptosis, promoted PTEN and P27 expression, and inhibited PI3K, P-Akt, and cyclin D1 expression at the protein level. Upregulation of miR-26a-5p attenuated the effects of GAS5 upregulation on the proliferation, cell cycle, and apoptosis of HCC cells and on the expression of PTNE/PI3K/Akt signaling pathway-related proteins. Conclusion Low GAS5 levels regulate the proliferation and apoptosis of HCC cells via the PTNE/PI3K/ Akt signaling pathway and are linked to upregulation of miR-26a-5p.
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