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首页> 外文期刊>Cellular Physiology and Biochemistry >CNTN-1 Enhances Chemoresistance in Human Lung Adenocarcinoma Through Induction of Epithelial-Mesenchymal Transition by Targeting the PI3K/Akt Pathway
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CNTN-1 Enhances Chemoresistance in Human Lung Adenocarcinoma Through Induction of Epithelial-Mesenchymal Transition by Targeting the PI3K/Akt Pathway

机译：CNTN-1通过靶向PI3K / Akt途径诱导上皮-间充质转化增强人肺腺癌的化学耐药性

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>Background/Aims: Chemoresistance has been a major obstacle to the effective treatment of lung cancer. Previously, we found that contactin-1 (CNTN-1) is related to cisplatin resistance in lung adenocarcinoma. Here, we aimed to investigate the underlying mechanism behind the role of CNTN-1 in cisplatin resistance in lung adenocarcinoma. Methods: EMT-associated phenotypes, including alterations in cellular morphology and marker (E-cadherin, N-cadherin and Vimentin) expression, were compared between A549 cells and A549/DDP cells (a cisplatin-resistant cell line of lung adenocarcinoma with abnormal CNTN-1 expression) by using real-time time PCR and Western blotting. Other methods, including CNTN-1 overexpression in A549 cells and CNTN-1 knockdown in A549/DDP cells, were also used to investigate the role of CNTN-1 in mediating the EMT phenotype and thr resulting cisplatin resistance and malignant progression of cancer cells in vitro and in vivo. Results: A549/DDP cells exhibited an EMT phenotype and aggravated malignant behaviors. CNTN-1 knockdown in A549/DDP cells partly reversed the EMT phenotype, increased drug sensitivity, and attenuated the malignant progression whereas CNTN-1 overexpression in A549 cells resulted in the opposite trend. Furthermore, the PI3K/Akt pathway was involved in the effects of CNTN-1 on EMT progression in A549/DDP cells, verified by the xenograft mouse model. Conclusion: CNTN-1 promotes cisplatin resistance in human cisplatin-resistant lung adenocarcinoma through inducing the EMT process by activating the PI3K/Akt signaling pathway. CNTN-1 may be a potential therapeutic target to reverse chemoresistance in cisplatin-resistant lung adenocarcinoma.
机译：> 背景/目标： 化学耐药性一直是有效治疗肺癌的主要障碍。以前，我们发现在肺腺癌中contactin-1（CNTN-1）与顺铂耐药性有关。在这里，我们旨在调查CNTN-1在肺腺癌中对顺铂耐药的作用背后的潜在机制。 方法： 比较了A549细胞和A549 / DDP与EMT相关的表型，包括细胞形态和标志物（E-钙粘蛋白，N-钙粘蛋白和波形蛋白）的表达变化。实时荧光定量PCR和Western印迹法检测细胞（CNTN-1表达异常的肺腺癌顺铂耐药细胞系）。其他方法，包括在A549细胞中过度表达CNTN-1和在A549 / DDP细胞中降低CNTN-1，也被用于研究CNTN-1在介导EMT表型和由此产生的顺铂耐药性以及癌细胞恶性进展中的作用。 i>体外和体内。 结果： A549 / DDP细胞表现出EMT表型并加重了恶性行为。 A549 / DDP细胞中的CNTN-1敲低部分逆转了EMT表型，增加了药物敏感性，并减弱了恶性进展，而A549细胞中CNTN-1的过表达导致了相反的趋势。此外，PI3K / Akt通路参与了CNTN-1对A549 / DDP细胞EMT进展的影响，这已通过异种移植小鼠模型进行了验证。 结论： CNTN-1通过激活PI3K / Akt信号传导途径诱导EMT进程，促进人对顺铂耐药的肺腺癌的顺铂耐药性。 CNTN-1可能是逆转对顺铂耐药的肺腺癌化学耐药性的潜在治疗靶标。

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