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长链非编码 RNA LINC00511 通过海绵吸附 miR-625-5p 调控 PKM2 表达，在肺腺癌中发挥致癌作用。

LncRNA LINC00511 plays an oncogenic role in lung adenocarcinoma by regulating PKM2 expression via sponging miR-625-5p.

机构信息

Medical ICU, Tianjin Hospital, Tianjin, China.

Heart Disease Department, Tianjin Academy of Traditional Chinese Medicine Affiliated Hospital, Tianjin, China.

出版信息

Thorac Cancer. 2020 Sep;11(9):2570-2579. doi: 10.1111/1759-7714.13576. Epub 2020 Jul 27.

DOI:10.1111/1759-7714.13576
PMID:32716147
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7471024/
Abstract

BACKGROUND

Lung adenocarcinoma (LAC) is the most prominent histological subtype of non-small cell lung cancer (NSCLC) with a high rate of mortality and metastasis. Accumulating evidence has shown that long non-coding RNAs (lncRNAs) play malfunctioning roles in the development of human tumors. Hence, this study aimed to determine the biological function of LINC00511 in LAC and to provide a novel diagnostic and therapeutic target for it.

METHODS

LINC00511 expression in LAC tissues and cell lines (H1299 and A549) were detected by real time-polymerase chain reaction (RT-qPCR). Cell counting kit-8 (CCK-8) assay was employed to analyze cell proliferative ability. Cell metastasis change was measured using transwell assay. Moreover, we revealed a novel target gene of LINC00511 and elucidated the underlying competitive endogenous RNA regulatory mechanism in LAC cells.

RESULTS

Data from our study demonstrated that LINC00511 expression was increased in LAC tissues and cells in comparison to their corresponding controls. Moreover, overexpression of LINC00511 indicated the poor prognosis of LAC patients. Overexpression of LINC00511 promoted proliferation, invasion and migration capacities of LAC cells. Moreover, LINC00511 promoted LAC progression via serving as a sponge of miR-625-5p and regulating PKM2 expression.

CONCLUSIONS

The present study showed that LINC00511 was involved in LAC progression by targeting miR-625-5p/PKM2, indicating that LINC00511/miR-625-5p/PKM2 may function as promising therapeutic targets for LAC.

摘要

背景

肺腺癌（LAC）是非小细胞肺癌（NSCLC）中最突出的组织学亚型，其死亡率和转移率较高。越来越多的证据表明，长链非编码 RNA（lncRNA）在人类肿瘤的发展中发挥着功能失调的作用。因此，本研究旨在确定 LINC00511 在 LAC 中的生物学功能，并为其提供新的诊断和治疗靶点。

方法

通过实时聚合酶链反应（RT-qPCR）检测 LAC 组织和细胞系（H1299 和 A549）中的 LINC00511 表达。使用细胞计数试剂盒-8（CCK-8）测定分析细胞增殖能力。通过 Transwell 测定法测量细胞转移变化。此外，我们揭示了 LINC00511 的一个新靶基因，并阐明了 LAC 细胞中竞争性内源性 RNA 调节机制的潜在机制。

结果

本研究数据表明，与相应对照相比，LAC 组织和细胞中的 LINC00511 表达增加。此外，LINC00511 的过表达表明 LAC 患者的预后不良。LINC00511 的过表达促进了 LAC 细胞的增殖、侵袭和迁移能力。此外，LINC00511 通过作为 miR-625-5p 的海绵和调节 PKM2 表达来促进 LAC 的进展。

结论

本研究表明，LINC00511 通过靶向 miR-625-5p/PKM2 参与 LAC 的进展，表明 LINC00511/miR-625-5p/PKM2 可能作为 LAC 的有前途的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75c1/7471024/617d9a03fba1/TCA-11-2570-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75c1/7471024/46a58a0961b1/TCA-11-2570-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75c1/7471024/49e5319097dc/TCA-11-2570-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75c1/7471024/11a0eb6f0ce1/TCA-11-2570-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75c1/7471024/841c362f5e9d/TCA-11-2570-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75c1/7471024/649a2a547c38/TCA-11-2570-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75c1/7471024/617d9a03fba1/TCA-11-2570-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75c1/7471024/46a58a0961b1/TCA-11-2570-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75c1/7471024/49e5319097dc/TCA-11-2570-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75c1/7471024/11a0eb6f0ce1/TCA-11-2570-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75c1/7471024/841c362f5e9d/TCA-11-2570-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75c1/7471024/649a2a547c38/TCA-11-2570-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75c1/7471024/617d9a03fba1/TCA-11-2570-g006.jpg

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