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长基因间非编码 RNA 对激酶激活(LINK-A)作为非小细胞肺癌致癌基因的作用。

The role of long intergenic non-coding RNA for kinase activation (LINK-A) as an oncogene in non-small cell lung carcinoma.

机构信息

Department of Molecular Medicine, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran.

Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran.

出版信息

Sci Rep. 2021 Feb 18;11(1):4210. doi: 10.1038/s41598-021-82892-z.

Abstract

The oncogenic role of long intergenic non-coding RNA for kinase activation (LINK-A) has been appraised in triple-negative breast cancer. However, the molecular function of LINK-A is still unclear in most cancers including lung cancer. The present study aimed to evaluate the impact of down-regulation of LINK-A in A549 and Calu-3 cell lines as cellular models of non-small cell lung carcinoma (NSCLC). We used the RNA interference system to knock down LINK-A. LINK-A expression was significantly reduced by siRNA transfection in A549 and Calu-3 cell lines. LINK-A down-regulation significantly reduced cell viability, colony-forming ability and cell migration, as measured by MTT, colony formation and invasion assays. Finally, cell cycle analysis and Annexin-V/7AAD staining indicated that apoptosis was influenced by LINK-A silencing. Taken together, LINK-A can be proposed as an oncogene in NSCLC.

摘要

长基因间非编码 RNA 对激酶激活 (LINK-A) 的致癌作用已在三阴性乳腺癌中得到评估。然而,在包括肺癌在内的大多数癌症中,LINK-A 的分子功能仍不清楚。本研究旨在评估下调 LINK-A 在 A549 和 Calu-3 细胞系(非小细胞肺癌 (NSCLC) 的细胞模型)中的影响。我们使用 RNA 干扰系统敲低 LINK-A。LINK-A 的表达通过 A549 和 Calu-3 细胞系中的 siRNA 转染显著降低。LINK-A 下调显著降低了 MTT、集落形成和侵袭测定法测量的细胞活力、集落形成和细胞迁移能力。最后,细胞周期分析和 Annexin-V/7AAD 染色表明,凋亡受 LINK-A 沉默的影响。总之,LINK-A 可以被提出作为 NSCLC 的致癌基因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c93b/7892821/55c6a6eff274/41598_2021_82892_Fig1_HTML.jpg

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