Krüppel-Like Factor 4 Enhances Sensitivity of Cisplatin to Lung Cancer Cells and Inhibits Regulating Epithelial-to-Mesenchymal Transition.
Krüppel-Like Factor 4 Enhances Sensitivity of Cisplatin to Lung Cancer Cells and Inhibits Regulating Epithelial-to-Mesenchymal Transition.
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DOI：
10.3727/096504016x14597766487717
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发表时间：
2016
影响因子：
3.1
通讯作者：
Chen Q
中科院分区：
文献类型：
--
作者：
Liu S;Yang H;Chen Y;He B;Chen Q
目前迫切需要了解肺癌细胞顺铂耐药的机制，以提高顺铂的治疗效果。本研究旨在探讨Krüppel样因子4（KLF 4）在肺癌顺铂耐药细胞中的作用。我们建立了肺癌顺铂耐药细胞系A549/DDP，并通过一系列实验研究了KLF 4在肺癌顺铂耐药中的作用。我们发现KLF 4在顺铂耐药的A549细胞中表达显著下调，并且强制表达KLF 4抑制细胞生长并诱导细胞凋亡。此外，我们发现KLF 4的过表达能够抑制细胞迁移和侵袭，抑制Slug，Twist和波形蛋白的表达，并增加E-cadherin的表达和随后的EMT过程的抑制。因此，KLF 4的过表达可能是肺癌治疗的一种潜在策略，特别是对于顺铂耐药病例。
In order to improve therapeutic efficacy, it is a current emergency to better know the mechanisms underlying cisplatin resistance in lung cancer cells. In this study, we aim to investigate the role of Krüppel-like factor 4 (KLF4) in cisplatin-resistant lung cancer cells. We developed cisplatin-resistant lung cancer cell line A549/DDP, and then a battery of experiments was used to analyze the effects of KLF4 in cisplatin resistance of lung cancer. We found that KLF4 was significantly downregulated in cisplatin-resistant A549 cells and forced KLF4 expression inhibited cell growth and induced apoptosis. Further, we found that overexpression of KLF4 was able to inhibit cell migration and invasion, to inhibit the expression of Slug, Twist, and vimentin, and to increase the expression of E-cadherin and subsequent inhibition of the EMT process. Thus, overexpression of KLF4 may be a potential strategy for lung cancer treatment, especially for cisplatin-resistant cases.