宫颈癌（CC）与持续性人乳头瘤病毒感染密切相关，是全世界女性的一个主要健康问题。本研究的目的是阐明KIF23在CC发生发展中的作用及其调控机制。利用生物信息学方法从GSE9750和GSE63678数据集中提取细胞焦亡相关的差异表达基因（DEG）和枢轴基因，然后进行免疫浸润对这些基因的表达进行分析和定量。驱动蛋白家族成员 23 (KIF23) 的作用已通过体外功能实验和小鼠异种移植模型得到验证。应用NLPR3激活剂尼日利亚菌素进一步分析KIF23在CC中的潜在调控机制，共筛选出8个与焦亡相关的DEG，其中4个候选核心基因被确定为候选枢纽基因，并证实在CC组织中上调和细胞。这些基因分别与不同免疫细胞的浸润或肿瘤纯度呈正相关。 KIF23的下调可以抑制CC细胞的增殖、迁移和侵袭能力，并通过增强焦亡来抑制肿瘤发生。相反，KIF23 过表达会加速 CC 细胞的恶性表型并抑制细胞焦亡激活，而尼日利亚菌素治疗可阻断这一激活。KIF23 可能通过抑制 NLRP3 介导的细胞焦亡途径在 CC 进展中发挥致癌作用。© 2024 美国实验学会联合会生物学。

Cervical cancer (CC), closely linked to persistent human papillomavirus infection, represents a major health problem for women worldwide. The objective of this study is to elucidate KIF23's role in the development of CC and its regulatory mechanism.The bioinformatics methods were utilized to extract pyroptosis-associated differentially expressed genes (DEGs) and pivot genes from the GSE9750 and GSE63678 datasets, followed by immune infiltration analysis and quantification of these genes' expression. The effects of kinesin family member 23 (KIF23) were verified through functional experiments in vitro and a mouse xenograft model. The NLPR3 activator, nigericin, was applied for further analyzing the potential regulatory mechanism of KIF23 in CC.A total of 8 pyroptosis-related DEGs were screened out, among which 4 candidate core genes were identified as candidate hub genes and confirmed upregulation in CC tissues and cells. These genes respectively showed a positive correlation with the infiltration of distinct immune cells or tumor purity. Downregulation of KIF23 could suppress the proliferation, migration, and invasion abilities in CC cells and tumorigenesis through enhancing pyroptosis. Conversely, KIF23 overexpression accelerated the malignant phenotypes of CC cells and inhibited pyroptosis activation, which was blocked by nigericin treatment.KIF23 may play an oncogenic role in CC progression via inhibition of the NLRP3-mediated pyroptosis pathway.© 2024 Federation of American Societies for Experimental Biology.