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NLRP3炎性小体在口腔鳞状细胞癌中的调控机制
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Abstract:
口腔鳞状细胞癌(OSCC)是头颈部最常见的恶性肿瘤，越来越多的证据强调炎症在OSCC进展中的重要性。急性和慢性炎症的主要信号通路包括NLR家族含pyrin结构域3 (NLRP3)炎性小体的激活，随后是胱天蛋白酶-1依赖性的促炎细胞因子IL-1β和IL-18的释放，以及由gasdermin-D介导细胞死亡。许多研究表明NLRP3炎性小体参与OSCC的发生，但是具体作用机制仍需进一步探索。因此，本文综述了NLRP3炎性小体的作用机制，并为开发新的OSCC治疗策略提供研究基础。
Oral squamous cell carcinoma (OSCC) is the most common malignant tumor in the head and neck, and increasing evidence emphasizes the importance of inflammation in the progression of OSCC. The main signaling pathways of acute and chronic inflammation include the activation of NLR family pyrin domain 3 (NLRP3) inflammasomes, followed by the caspase-1-dependent pro-inflammatory cytokine IL-1β and the release of IL-18, as well as cell death mediated by gasdermin-D. Many studies have shown that NLRP3 inflammasomes are involved in the occurrence of OSCC, but the specific mechanism of action still needs further exploration. Therefore, this article reviews the mechanism of action of NLRP3 inflammasome and provides a research basis for the development of new OSCC treatment strategies.
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