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长链非编码 RNA Linc01296 通过调节 miR-26a/PTEN 轴促进肝癌发展。

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

机构信息

Department of Thoracic Surgery, First People's Hospital of Yunnan Province, Kunming 650031, China.

Department of Medical Oncology, First People's Hospital of Yunnan Province, Kunming 650031, China.

出版信息

Biol Chem. 2020 Feb 25;401(3):407-416. doi: 10.1515/hsz-2019-0231.

DOI:10.1515/hsz-2019-0231
PMID:31318685
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.

摘要

长链非编码 RNA 01296(Lnc01296)在恶性肿瘤中失调。然而,Linc01296 对肝细胞癌(HCC)的详细影响在很大程度上仍然未知。在本研究中,我们确定了 Linc01296 在 HCC 中的生物学作用。通过实时定量聚合酶链反应(qRT-PCR)评估 HCC 组织和一系列细胞系中 Linc01296 的水平。使用细胞计数试剂盒-8(CCK-8)、流式细胞术、迁移和 Transwell 侵袭测定法探索 Linc01296 对 HCC 进展的影响。使用荧光素酶、RNA 免疫沉淀(RIP)和 Western blot 测定法确定 Linc01296、miR-26a 和 PTEN 之间的相互作用。利用肿瘤异种移植模型证实了 Linc01296 在 HCC 发展中的体内功能作用。Linc01296 在 HCC 组织样本和细胞系中均表达增加。Linc01296 的敲低抑制了 HCC 细胞的增殖、迁移和侵袭等过程,并在体外增强了细胞凋亡;这些作用可被 miR-26a 模拟物或 PTEN 过表达逆转。此外,Linc01296 的敲低抑制了 HCC 在体内的生长。这些发现表明,Linc01296 通过调节 miR-26a/PTEN 参与 HCC 进展。

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