Suppr超能文献

睾丸发育相关基因 1 通过 microRNA-214-5p/Krüppel 样因子 5 轴促进非小细胞肺癌。

Testis developmental related gene 1 promotes non-small-cell lung cancer through the microRNA-214-5p/Krüppel-like factor 5 axis.

机构信息

Soochow University, Suzhou, Jiangsu, China.

Department of Pulmonary and Critical Care Medicine, Affiliated Kunshan Hospital of Jiangsu University, Kunshan, Jiangsu, China.

出版信息

Bioengineered. 2022 Jan;13(1):603-616. doi: 10.1080/21655979.2021.2012406.

Abstract

Non-small-cell lung cancer (NSCLC) is a frequent malignancy and has a high global incidence. Long noncoding RNAs (lncRNAs) are implicated in carcinogenesis and tumor progression. LncRNA testis developmental related gene 1 (TDRG1) plays a pivotal role in many cancers. This study researched the biological regulatory mechanisms of TDRG1 in NSCLC. Gene expression was assessed by reverse transcriptase quantitative polymerase chain reaction (RT-qPCR). Changes in the NSCLC cell phenotypes were examined using 5-ethynyl-2'-deoxyuridine (EdU), cell counting kit-8 (CCK-8), wound healing, flow cytometry, and Transwell assays. The binding capacity between TDRG1, microRNA-214-5p (miR‑214-5p), and Krüppel-like factor 5 (KLF5) was tested using luciferase reporter and RNA immunoprecipitation (RIP) assays. In this study, we found that TDRG1 was upregulated in NSCLC samples. Functionally, TDRG1 depletion inhibited NSCLC cell growth, migration, and invasion and accelerated apoptosis. In addition, TDRG1 interacted with miR-214-5p, and miR-214-5p directly targeted KLF5. The suppressive effect of TDRG1 knockdown on NSCLC cellular processes was abolished by KLF5 overexpression. Overall, TDRG1 exerts carcinogenic effects in NSCLC by regulating the miR-214-5p/KLF5 axis.

摘要

非小细胞肺癌(NSCLC)是一种常见的恶性肿瘤,具有很高的全球发病率。长链非编码 RNA(lncRNA)参与了致癌作用和肿瘤进展。lncRNA 睾丸发育相关基因 1(TDRG1)在许多癌症中发挥着关键作用。本研究研究了 TDRG1 在 NSCLC 中的生物学调节机制。通过逆转录定量聚合酶链反应(RT-qPCR)评估基因表达。通过 5-乙炔基-2'-脱氧尿苷(EdU)、细胞计数试剂盒-8(CCK-8)、划痕愈合、流式细胞术和 Transwell 测定来检测 NSCLC 细胞表型的变化。通过荧光素酶报告和 RNA 免疫沉淀(RIP)测定来测试 TDRG1、microRNA-214-5p(miR-214-5p)和 Krüppel 样因子 5(KLF5)之间的结合能力。在本研究中,我们发现 TDRG1 在 NSCLC 样本中上调。功能上,TDRG1 耗竭抑制 NSCLC 细胞生长、迁移和侵袭并加速细胞凋亡。此外,TDRG1 与 miR-214-5p 相互作用,miR-214-5p 直接靶向 KLF5。KLF5 过表达消除了 TDRG1 敲低对 NSCLC 细胞过程的抑制作用。总之,TDRG1 通过调节 miR-214-5p/KLF5 轴在 NSCLC 中发挥致癌作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1216/8805868/19454e7ec1ad/KBIE_A_2012406_UF0001_OC.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验