食管鳞癌细胞自分泌白介素-32通过诱导上皮间质转化促进肿瘤恶性表型  

Autocrine interleukin-32 from esophageal squamous cell carcinoma cells promotes malignant phenotype of cancer cells via inducing epithelial-mesenchymal transition

作　　者：杨昕 徐晓琴[1,4] 孔鹏洲 YANG Xin;XU Xiaoqin;KONG Pengzhou(Translational Medicine Research Center,Shanxi Medical University,Shanxi Taiyuan 030001,China;Key Laboratory of Cell Physiology,Ministry of Education,Shanxi Medical University,Shanxi Taiyuan 030001,China;Department of Pathology,Shanxi Medical University,Shanxi Taiyuan 030001,China;Department of Etiology,Cancer Institute,Shanxi Provincial Cancer Hospital,Shanxi Taiyuan 030000,China)

机构地区：[1]山西医科大学转化医学研究中心,山西太原030001 [2]山西医科大学细胞生理学教育部重点实验室,山西太原030001 [3]山西医科大学病理教研室,山西太原030001 [4]山西省肿瘤医院肿瘤研究所病因室,山西太原030000

出　　处：《现代肿瘤医学》2022年第12期2114-2119,共6页Journal of Modern Oncology

基　　金：国家自然科学基金项目(编号:82072746)。

摘　　要：目的:探讨食管鳞癌(esophageal squamous cell carcinoma,ESCC)细胞自分泌的白介素-32(interleukin-32,IL-32)对细胞恶性表型的影响及其可能机制。方法:分析ESCC组织和正常组织中IL-32表达量差异,检测不同ESCC细胞系中IL-32表达;在高表达细胞中利用siRNA敲低IL-32表达,在低表达细胞系中过表达IL-32;通过MTT、Transwell实验等检测IL-32对ESCC细胞增殖、侵袭、迁移等表型的影响;Western blot检测上皮间质转化相关基因的表达变化。结果:ESCC组织中IL-32的表达量显著高于正常组织,ESCC细胞系中IL-32的表达量显著高于食管上皮永生化细胞系Het-1A;敲低IL-32显著抑制ESCC细胞的增殖、迁移和侵袭能力,过表达IL-32促进ESCC细胞的恶性表型;Western blot结果显示IL-32促进ESCC细胞发生上皮间质转化。结论:ESCC细胞自分泌的IL-32可能通过促进ESCC细胞发生上皮间质转化从而发挥促癌作用,抑制IL-32可能成为治疗ESCC的一种方法。Objective:To investigate the effect of autocrine interleukin-32(IL-32)on the malignant phenotype of esophageal squamous cell carcinoma(ESCC).Methods:IL-32 expression in ESCC tissues and normal tissues was compared.IL-32 expression was detected in different ESCC cell lines.IL-32 was knock down and overexpressed in high and low expression cell lines respectively,and the effects of IL-32 on malignant phenotype of ESCC cells were detected by MTT,Transwell invasion and migration experiments.Western blot detected the expression of epithelial-mesenchymal transition(EMT)related genes.Results:IL-32 expression was significantly higher in ESCC tissues than that in the normal tissues.IL-32 expression in ESCC cell lines was significantly higher than that in Het-1A.Down-regulation of IL-32 significantly inhibited the proliferation,migration and invasion of ESCC cells,while overexpression of IL-32 promoted the proliferation,migration and invasion of ESCC cells.Western blot showed IL-32 promoted EMT in ESCC cells.Conclusion:IL-32 promotes the malignant phenotypes of ESCC cells via promoting EMT,and inhibition of IL-32 could act as a potential method to treat ESCC.

关 键 词：食管鳞癌 白介素-32 侵袭 迁移 上皮间质转化 

分 类 号：R735.1[医药卫生—肿瘤]