Cisplatin Induces Pyroptosis via Activation of MEG3/NLRP3/caspase-1/GSDMD Pathway in Triple-Negative Breast Cancer

上睑下垂 基因敲除 乙二醇 癌症研究 雷公藤甲素 细胞凋亡 信号转导 乳腺癌 程序性细胞死亡 顺铂 转移 化学 机制(生物学) 生物 下调和上调 RNA干扰 癌症 抑制器 基因沉默 癌细胞 小RNA 自噬 医学
作者
Honglin Yan,Bin Luo,Xiaoyan Wu,Feng Guan,Xinxin Yu,Lina Zhao,Xiaokang Ke,Juan Wu,Jingping Yuan
出处
期刊:International Journal of Biological Sciences [Ivyspring International Publisher]
卷期号:17 (10): 2606-2621 被引量:265
标识
DOI:10.7150/ijbs.60292
摘要

Cisplatin (DDP) was reported to improve pathological complete response (pCR) rates in triple-negative breast cancer (TNBC) patients, however, the molecular mechanism still remains largely unknown. Emerging evidence suggested that some chemotherapeutic drugs played anti-tumor effects by inducing cell pyroptosis. Nevertheless, whether pyroptosis contributes to the DDP-induced anti-tumor effect in TNBC remains unexploited. In the present study, NLRP3/caspase-1/GSDMD pyroptosis pathway was involved in the DDP-induced anti-tumor effect of TNBC in vitro and in vivo, providing evidence that DDP might induce pyroptosis in TNBC. Moreover, DDP activated NLRP3/caspase-1/GSDMD pyroptosis pathway by up-regulating the long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3). Furthermore, knockdown of MEG3 not only partly abolished the activation effect of DDP on NLRP3/caspase-1/GSDMD pathway-mediated pyroptosis, but also reversed the suppression of DDP on tumor growth and metastasis ability in vitro and in vivo, further confirming that MEG3 may partially mediate the pyroptotic signaling upon DDP treatment. Thus, our data uncovered a novel mechanism that DDP induced pyroptosis via activation of MEG3/NLRP3/caspase-1/GSDMD pathway in TNBC to exert anti-tumor effects, which may help to develop new strategies for the therapeutic interventions in TNBC.
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