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长链非编码RNA CASC2通过下调miR-18a和miR-21来调节PTEN/PI3K/Akt通路，从而增强顺铂诱导的非小细胞肺癌细胞活力抑制作用。

Long non-coding RNA CASC2 enhanced cisplatin-induced viability inhibition of non-small cell lung cancer cells by regulating the PTEN/PI3K/Akt pathway through down-regulation of miR-18a and miR-21.

作者信息

Li Li, Zhang Haifeng, Wang Xiaolong, Wang Jiali, Wei Haitao

机构信息

School of Nursing and Health, Henan University Kaifeng 475004 P. R. China.

Department of Thoracic Surgery, Huaihe Hospital of Henan University Baobei Road No. 8 Kaifeng 475000 P. R. China

出版信息

RSC Adv. 2018 Apr 30;8(29):15923-15932. doi: 10.1039/c8ra00549d. eCollection 2018 Apr 27.

DOI:10.1039/c8ra00549d
PMID:35542225
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9080181/
Abstract

Long non-coding RNA cancer susceptibility candidate 2 (lncRNA CASC2) is a tumor suppressor and has been proved to contribute to chemotherapy efficacy. However, the effect of CASC2 on cisplatin cytotoxicity in non-small cell lung cancer (NSCLC) is unclear. The present study aimed to investigate the role of CASC2 in regulating cisplatin cytotoxicity in NSCLC cells. Herein, we found that CASC2 was low-expressed, while miR-18a and miR-21 were over-expressed in NSCLC cell lines. CASC2 enhanced the inhibition effect of cisplatin on cell viability. Down-regulation of miR-18a and miR-21 exhibited the similar effect to CASC2 and mimics of miR-18a and miR-21 displayed the opposite effect to CASC2. MiR-18a and miR-21 were two targets of CASC2 in NSCLC. PTEN was found to be a target of miR-18a and miR-21 in NSCLC. CASC2 overexpression increased PTEN expression level and reduced the ratio of p-Akt/Akt. MiR-18a or miR-21 mimics attenuated the effect of CASC2 overexpression on the PTEN expression and ratio of p-Akt/Akt. The results suggested that CASC2 enhanced cisplatin-induced viability inhibition of NSCLC cells PTEN/PI3K/Akt pathway through suppressing miR-18a and miR-21 expression.

摘要

长链非编码RNA癌症易感性候选基因2（lncRNA CASC2）是一种肿瘤抑制因子，已被证明有助于提高化疗疗效。然而，CASC2对非小细胞肺癌（NSCLC）顺铂细胞毒性的影响尚不清楚。本研究旨在探讨CASC2在调节NSCLC细胞顺铂细胞毒性中的作用。在此，我们发现CASC2在NSCLC细胞系中低表达，而miR-18a和miR-21高表达。CASC2增强了顺铂对细胞活力的抑制作用。下调miR-18a和miR-21表现出与CASC2相似的作用，而miR-18a和miR-21模拟物则表现出与CASC2相反的作用。在NSCLC中，miR-18a和miR-21是CASC2的两个靶点。发现PTEN是NSCLC中miR-18a和miR-21的靶点。CASC2过表达增加了PTEN表达水平，并降低了p-Akt/Akt的比值。miR-18a或miR-21模拟物减弱了CASC2过表达对PTEN表达和p-Akt/Akt比值的影响。结果表明，CASC2通过抑制miR-18a和miR-21的表达增强顺铂诱导的NSCLC细胞活力抑制 PTEN/PI3K/Akt通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8213/9080181/53842af45e18/c8ra00549d-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8213/9080181/7eefe380935a/c8ra00549d-f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8213/9080181/c4cb8b0d19cb/c8ra00549d-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8213/9080181/7a8ea45154c2/c8ra00549d-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8213/9080181/a08d6dd281fe/c8ra00549d-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8213/9080181/53842af45e18/c8ra00549d-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8213/9080181/7eefe380935a/c8ra00549d-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8213/9080181/0034e7000e40/c8ra00549d-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8213/9080181/1bcd40e89a2c/c8ra00549d-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8213/9080181/c4cb8b0d19cb/c8ra00549d-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8213/9080181/7a8ea45154c2/c8ra00549d-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8213/9080181/a08d6dd281fe/c8ra00549d-f6.jpg
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