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脂联素通过逆转非小细胞肺癌中的上皮-间质转化抑制迁移和侵袭。

Adiponectin inhibits migration and invasion by reversing epithelial‑mesenchymal transition in non‑small cell lung carcinoma.

机构信息

Department of Respiratory Medicine, Huzhou Central Hospital, Huzhou, Zhejiang 313000, P.R. China.

Center of Clinical Laboratory, The First People's Hospital of Huzhou, Huzhou Teachers College, Huzhou, Zhejiang 313000, P.R. China.

出版信息

Oncol Rep. 2018 Sep;40(3):1330-1338. doi: 10.3892/or.2018.6523. Epub 2018 Jun 25.

Abstract

Adiponectin is the most abundant adipokine in the tumor microenvironment. The role of this protein in tumor progression, however, remains controversial. In the present study, we aimed to investigate the effects of adiponectin on the abilities of migration and invasion in non‑small cell lung carcinoma (NSCLC). Using NSCLC cell lines, we examined the effects of adiponectin on cell migration and invasion using Transwell assays. Expression of epithelial‑mesenchymal transition markers was examined via microscopy and western blotting. We also performed a knockdown of Twist, AdipoR1 and AdipoR2 in NSCLC cells with siRNAs. The addition of adiponectin to NSCLC cells inhibited both the migration and invasion abilities. Furthermore, we found that NSCLC cells displayed increased epithelial marker expression and downregulation of mesenchymal marker expression following adiponectin administration. Twist AdipoR1 and AdipoR2 knockdown reversed the inhibitory effects of adiponectin on migration and invasion in NSCLC and epithelial‑mesenchymal transition. Exogenous adiponectin significantly impaired the migratory and invasive capacities of NSCLC cells through reversal of EMT, suggesting that adiponectin may be a novel promising therapeutic approach against NSCLC.

摘要

脂联素是肿瘤微环境中含量最丰富的脂肪因子。然而,这种蛋白质在肿瘤进展中的作用仍存在争议。在本研究中,我们旨在研究脂联素对非小细胞肺癌(NSCLC)迁移和侵袭能力的影响。使用 NSCLC 细胞系,我们通过 Transwell 分析检测脂联素对细胞迁移和侵袭的影响。通过显微镜和 Western blot 检测上皮-间充质转化标志物的表达。我们还通过 siRNA 在 NSCLC 细胞中敲低 Twist、AdipoR1 和 AdipoR2。向 NSCLC 细胞中添加脂联素抑制了迁移和侵袭能力。此外,我们发现脂联素处理后 NSCLC 细胞中上皮标志物表达增加,间充质标志物表达下调。Twist、AdipoR1 和 AdipoR2 的敲低逆转了脂联素对 NSCLC 和上皮-间充质转化中迁移和侵袭的抑制作用。外源性脂联素通过逆转 EMT 显著削弱 NSCLC 细胞的迁移和侵袭能力,提示脂联素可能是一种有前途的 NSCLC 治疗新方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8ba/6072398/bc6acf5023f1/OR-40-03-1330-g00.jpg

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