Cisplatin has strong broad‐spectrum anticancer activity and is one of the most effective anticancer drugs currently used. The clinical application of cisplatin has led to the resistance of cancer cells to cisplatin. Tachyplesin is an active, natural marine peptide with antitumour activity. In the present study, we investigated whether tachyplesin can be used in non‐small cell lung cancer (NSCLC) A549 and H460 cells as well as the cisplatin‐resistant human A549/DDP NSCLC cell line. The results revealed that tachyplesin treatment significantly inhibited proliferation and induced apoptosis in A549 and H460 cells and the combination of tachyplesin and cisplatin significantly suppressed migration and improved sensitivity to cisplatin in A549/DDP cells. Further mechanistic examination revealed that tachyplesin induced apoptosis in A549/DDP cells by increasing Fas, FasL and p‐RIPK1 levels. These results indicated that tachyplesin induces lung cancer death by activating the Fas, mitochondrial and necroptosis pathways. Tachyplesin could be developed as a candidate drug for cisplatin‐resistant NSCLC.

中文翻译：

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Tachyplesin 通过激活 Fas 和坏死性凋亡通路诱导非小细胞肺癌细胞凋亡并增强 A549/DDP 细胞对顺铂的化学敏感性

顺铂具有很强的广谱抗癌活性，是目前使用最有效的抗癌药物之一。顺铂的临床应用导致癌细胞对顺铂产生耐药性。Tachyplesin 是一种具有抗肿瘤活性的活性天然海洋肽。在本研究中，我们研究了 tachyplesin 是否可用于非小细胞肺癌 (NSCLC) A549 和 H460 细胞以及顺铂耐药的人 A549/DDP NSCLC 细胞系。结果表明，tachyplesin 处理显着抑制 A549 和 H460 细胞的增殖并诱导细胞凋亡，tachyplesin 和顺铂的组合显着抑制了 A549/DDP 细胞的迁移并提高了对顺铂的敏感性。进一步的机制检查表明，速效素通过增加 Fas、FasL 和 p-RIPK1 水平诱导 A549/DDP 细胞凋亡。这些结果表明 tachyplesin 通过激活 Fas、线粒体和坏死性凋亡途径诱导肺癌死亡。Tachyplesin 可以开发为顺铂耐药 NSCLC 的候选药物。