EZH2–STAT3 signaling pathway regulates GSDMD-mediated pyroptosis in glioblastoma

上睑下垂 梅尔特克 癌症研究 车站3 生物 信号转导 细胞生物学 免疫学 炎症体 炎症 受体酪氨酸激酶
作者
Dong Yu,Shuai Wang,Sheng Wang,Kang Zhang,Zhisheng Niu,Ning Lin
出处
期刊:Cell death discovery [Springer Nature]
卷期号:10 (1)
标识
DOI:10.1038/s41420-024-02105-0
摘要

Abstract Glioblastoma multiforme (GBM) is the most therapeutically challenging primary brain tumor owing to the unique physiological structure of the blood–brain barrier. Lately, research on targeted therapy for gliomas has shifted focus toward the tumor microenvironment and local immune responses. Pyroptosis is a newly identified cellular demise characterized by the release of numerous inflammatory factors. While pyroptosis shows promise in impeding the occurrence and progression of GBM, the regulatory mechanisms governing this process in gliomas still require further investigation. The function of the Enhancer of zeste homolog 2 (EZH2) in pyroptosis remains unexplored. In this study, we discovered that 3-Deazaneplanocin A (DZNep), an inhibitor of EZH2, can induce pyroptosis in GBM in vitro experiments. Moreover, our investigation unveiled that the signal transducer and activator of transcription (STAT3) could serve as a downstream regulator influenced by EZH2, impacting pyroptosis in GBM. Following treatment with DZNep and the STAT3 inhibitor (SH-4–54), there was an elevation in the levels of pyroptosis-related factors, namely NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) and Gasdermin D (GSDMD). Moreover, simultaneous inhibition of both EZH2 and STAT3 led to the expression of inflammatory factors such as IL-1β and IL-18. In summary, we have identified that EZH2 regulates pyroptosis in GBM through STAT3, and pyroptosis could potentially be targeted for immunotherapy in GBM.

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