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NLRP3 炎性小体在口腔鳞状细胞癌中的作用
Authors Shi R, Zhuang X, Liu T, Yao SN, Xue FS
Received 17 December 2024
Accepted for publication 21 March 2025
Published 25 April 2025 Volume 2025:18 Pages 5601—5609
DOI http://doi.org/10.2147/JIR.S512770
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Professor Ning Quan
Rui Shi,1,2 Xuan Zhuang,3 Tong Liu,4 Song-nan Yao,3 Feng-shan Xue3
1Department of Oral and Maxillofacial Reconstruction, The Affiliated Hospital of Qingdao University 266600, Qingdao, 266555, People’s Republic of China; 2School of Stomatology of Qingdao University, Qingdao, 266555, People’s Republic of China; 3Cardiac Surgery Intensive Care Unit Department, the Affiliated Hospital of Qingdao University, Qingdao, 266555, People’s Republic of China; 4The Affiliated Tai’an City Central Hospital of Qingdao University, Taian, 271000, People’s Republic of China
Correspondence: Song-nan Yao, Cardiac Surgery Intensive Care Unit Department of the affiliated hospital of Qingdao University 266600, Qingdao, People’s Republic of China, Email yaosongnan@qdu.edu.cn Feng-shan Xue, Cardiac Surgery Intensive Care Unit Department of the affiliated hospital of Qingdao University 266600, Qingdao, People’s Republic of China, Email 15166616637@163.com
Background: Oral squamous cell carcinoma (OSCC) is the most common malignant tumor in the head and neck. More and more evidence emphasizes the importance of inflammation in the progression of OSCC. The main signaling pathway of acute and chronic inflammation consists of the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome.
Objective: This review focuses on the role of NLRP3 immune kinase body and giving a contribution to the development of new treatment strategies against OSCC.
Conclusion: The NLRP3 inflammasome plays a vital role in the pathogenesis and development of OSCC and may serve as a promising therapeutic target for autoimmune diseases.
Keywords: NLRP31, oral squamous cell carcinoma 2, Caspase-13, GSDMD4, autophagy5