Startseite Long noncoding RNA Linc01296 promotes hepatocellular carcinoma development through regulation of the miR-26a/PTEN axis
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Long noncoding RNA Linc01296 promotes hepatocellular carcinoma development through regulation of the miR-26a/PTEN axis

  • Libin Zhang , Jing Hu , Menghui Hao EMAIL logo und Liang Bu EMAIL logo
Veröffentlicht/Copyright: 18. Juli 2019

Abstract

Long noncoding RNA 01296 (Lnc01296) is dysregulated in malignant tumors. However, the detailed effect of Linc01296 on hepatocellular carcinoma (HCC) remains largely unknown. In this study, we identified the biological role of Linc01296 in HCC. The levels of Linc01296 in HCC tissues and a panel of cell lines were assessed by quantitative real-time polymerase chain reaction (qRT-PCR). The effects of Linc01296 on HCC progression were explored using a Cell Counting Kit-8 (CCK-8), flow cytometry, migration and Transwell invasion assays. The interactions among Linc01296, miR-26a and PTEN were determined using luciferase, RNA immunoprecipitation (RIP) and Western blot assays. Tumor xenograft models were utilized to confirm the in vivo functional roles of Linc01296 in HCC development. Linc01296 expression was increased in both HCC tissue samples and cell lines. Knockdown of Linc01296 suppressed HCC cell processes, such as proliferation, migration and invasion, and enhanced apoptosis in vitro; these effects were reversed by a miR-26a mimic or PTEN overexpression. Furthermore, knockdown of Linc01296 suppressed HCC growth in vivo. These findings indicated that Linc01296 is involved in HCC progression via regulating miR-26a/PTEN.

Award Identifier / Grant number: 2017ZF026

Award Identifier / Grant number: 2017NS256

Funding statement: This project was supported by a grant from Huimin Special Science and Technology (No. 2017ZF026) and the medical and health units of research institutions for scientific research projects in Yunnan Province (No. 2017NS256).

  1. Conflict of interest statement: The authors declare no conflicts of interest.

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Received: 2019-04-21
Accepted: 2019-07-09
Published Online: 2019-07-18
Published in Print: 2020-02-25

©2020 Walter de Gruyter GmbH, Berlin/Boston

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