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抑制长链非编码 RNA KCNQ1OT1 通过 TGF-β1 介导的上皮间质转化改善小细胞肺癌细胞的凋亡和化疗药物反应。

Inhibition of lncRNA KCNQ1OT1 Improves Apoptosis and Chemotherapy Drug Response in Small Cell Lung Cancer by TGF-β1 Mediated Epithelial-to-Mesenchymal Transition.

机构信息

Department of Pathology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.

Department of Medical Oncology, Provincial Clinical College, Fujian Medical University, Fujian provincial hospital, Fuzhou, China.

出版信息

Cancer Res Treat. 2021 Oct;53(4):1042-1056. doi: 10.4143/crt.2020.1208. Epub 2021 Mar 9.

DOI:10.4143/crt.2020.1208
PMID:33705625
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8524015/
Abstract

PURPOSE

Drug resistance is one of the main causes of chemotherapy failure in patients with small cell lung cancer (SCLC), and extensive biological studies into chemotherapy drug resistance are required.

MATERIALS AND METHODS

In this study, we performed lncRNA microarray, in vitro functional assays, in vivo models and cDNA microarray to evaluate the impact of lncRNA in SCLC chemoresistance.

RESULTS

The results showed that KCNQ1OT1 expression was upregulated in SCLC tissues and was a poor prognostic factor for patients with SCLC. Knockdown of KCNQ1OT1 inhibited cell proliferation, migration, chemoresistance and promoted apoptosis of SCLC cells. Mechanistic investigation showed that KCNQ1OT1 can activate transforming growth factor-β1 mediated epithelial-to-mesenchymal transition in SCLC cells.

CONCLUSION

Taken together, our study revealed the role of KCNQ1OT1 in the progression and chemoresistance of SCLC, and suggested KCNQ1OT1 as a potential diagnostic and prognostic biomarker in SCLC clinical management.

摘要

目的

耐药性是小细胞肺癌（SCLC）患者化疗失败的主要原因之一，需要对化疗药物耐药性进行广泛的生物学研究。

材料和方法

本研究通过 lncRNA 微阵列、体外功能测定、体内模型和 cDNA 微阵列来评估 lncRNA 在 SCLC 化疗耐药性中的作用。

结果

结果表明，KCNQ1OT1 在 SCLC 组织中表达上调，是 SCLC 患者的不良预后因素。敲低 KCNQ1OT1 抑制 SCLC 细胞的增殖、迁移、化疗耐药性，并促进细胞凋亡。机制研究表明，KCNQ1OT1 可以激活 SCLC 细胞中的转化生长因子-β1 介导的上皮间质转化。

结论

综上所述，本研究揭示了 KCNQ1OT1 在 SCLC 进展和化疗耐药性中的作用，并提示 KCNQ1OT1 可作为 SCLC 临床管理中潜在的诊断和预后生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efe/8524015/e5c6349a305d/crt-2020-1208f8.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efe/8524015/1579e7766052/crt-2020-1208f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efe/8524015/1f3e8d37d1a1/crt-2020-1208f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efe/8524015/eec95c9289e0/crt-2020-1208f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efe/8524015/e5c6349a305d/crt-2020-1208f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efe/8524015/bf74b21694a7/crt-2020-1208f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efe/8524015/1d38ae7a97e5/crt-2020-1208f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efe/8524015/de2dcc90d2b7/crt-2020-1208f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efe/8524015/1447ae088d60/crt-2020-1208f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efe/8524015/1579e7766052/crt-2020-1208f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efe/8524015/1f3e8d37d1a1/crt-2020-1208f6.jpg
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