临床与实验病理学杂志2026，Vol.42Issue(1)：29-37,9.DOI:10.13315/j.cnki.cjcep.2026.01.005
FOXK1通过上调ROCK1表达促进食管鳞状细胞癌的恶性生物学行为
FOXK1 promotes the malignant biological behavior of esophageal squamous cell carcinoma by upregulating ROCK1 expression
摘要
Abstract
Objective To investigate the expression,biological function,and underlying molecular mechanisms of FOXK1 in esophageal squamous cell carcinoma(ESCC).Methods ESCC cell lines KYSE-150,KYSE-170,and TE-1 were routinely cultured.Nucleic acids and plasmids were transfected into cells using transfection reagents.Data-base analysis combined with qRT-PCR was applied to determine FOXK1 expression in ESCC tissues and cells.Bioin-formatics analysis was used to predict downstream targets,with ROCK1 identified as a candidate.ROCK1 expression was examined by qRT-PCR,and a dual-luciferase reporter assay was proformed to confirm FOXK1-mediated transcrip-tional regulation of the ROCK1 promoter.Colony formation,wound-healing,and Transwell assays were conducted to evaluate cell proliferation,migration,and invasion.qRT-PCR and Western blotting were used to examine the expres-sion of epithelial-mesenchymal transition(EMT)-related markers,while immunofluorescence was applied to assess F-actin polymerization.Results FOXK1 expression was significantly upregulated in ESCC tissues and cell lines.In KYSE-150,KYSE-170,and TE-1 cells,FOXK1 expression was approximately 40.0-,17.9-,and 24.8-fold higher than that in normal esophageal epithelial cells,respectively(P<0.05).ROCK1 expression positively correlated with FOXK1 levels(P<0.05),and was also elevated in ESCC cells.FOXK1 overexpression increased,whereas FOXK1 knockdown decreased ROCK1 expression.Dual-luciferase reporter assays confirmed that FOXK1 directly bound to and activated the ROCK1 promoter.Functionally,ROCK1 overexpression enhanced ESCC cell proliferation,migration,and invasion,while ROCK1 knockdown inhibited these phenotypes.Co-manipulation of FOXK1 and ROCK1 partially reversed the pro-tumor effects of FOXK1 overexpression.Mechanistically,ROCK1 knockdown down-regulated the mRNA and protein expression of EMT markers(CDH2,vimentin,and ZEB1).FOXK1 overexpression promoted F-actin polymerization,whereas ROCK1 knockdown suppressed it;co-manipulation partially counteracted FOXK1-induced F-actin polymerization.Conclusion FOXK1 promotes ESCC cell migration and invasion by tran-scriptionally upregulating ROCK1,indicating that FOXK1 may serve as a potential diagnostic and therapeutic target in ESCC.关键词
食管肿瘤/鳞状细胞癌/FOXK1/ROCK1/上皮-间质转化/细胞骨架Key words
esophageal neoplasms/squamous cell carcinoma/FOXK1/ROCK1/epithelial-mesenchymal transition/cytoskeleton分类
医药卫生引用本文复制引用
武俊红,杨霞,许环琛,王歆皓,胡照坤,路军涛,郭炜..FOXK1通过上调ROCK1表达促进食管鳞状细胞癌的恶性生物学行为[J].临床与实验病理学杂志,2026,42(1):29-37,9.基金项目
河北省政府资助临床医学优秀人才培养项目(ZF2024099) The Project for Cultivating Outstanding Clinical Medical Talents Funded by the Hebei Provincial Government(ZF2024099) （ZF2024099）
