S100A2调控卵巢癌SKOV3/A2780细胞增殖和上皮间质转化的研究

Regulation of ovarian cancer SKOV3/A2780 cell proliferation and epithelial-mesenchymal transition by S100A2

目的探讨S100A2在调节卵巢癌(OC)细胞SKOV3/A2780的增殖和上皮-间质转化(EMT)过程中的作用。方法从GEO数据库下载GSE14407和GSE40595基因表达数据集。通过R软件筛选差异基因S100A2。培养上皮性OC细胞系SKOV3/A2780进行体外实验,并利用siRNA、质粒过表达、RT-qPCR、MTT法等技术,对S100A2在SKOV3/A2780细胞中的表达及功能进行研究。结果S100A2在SKOV3/A2780细胞中表达水平较高。进一步的功能实验显示,敲低S100A2抑制了细胞增殖,降低了EMT的程度。相反,过表达S100A2增强了细胞增殖,并促进了EMT的过程。机制上,干预S100A2的表达能够影响Wnt/β-catenin信号通路的相关基因。结论本研究揭示了S100A2在调控OC细胞系SKOV3/A2780生物学特性中的作用,为进一步理解OC的发病机制以及潜在治疗靶点提供了新的视角。

Objective To investigate the role of S100A2 in regulating proliferation and epithelial-to-mesenchymal transition(EMT)processes in ovarian cancer(OC)cells SKOV3/A2780.Methods Gene expression datasets GSE14407 and GSE40595 were downloaded from the GEO database.Differential expression of S100A2 was identified using R software.In vitro experiments were conducted using epithelial OC cell lines SKOV3/A2780.Techniques such as siRNA,plasmid overexpression,RT-qPCR,and MTT assay were employed to study the expression and function of S100A2 in SKOV3/A2780 cells.Results Experimental result demonstrated higher expression levels of S100A2 in SKOV3/A2780 cells.Further functional assays revealed that knocking down S100A2 inhibited cell proliferation and reduced EMT.Conversely,overexpression of S100A2 enhanced cell proliferation and facilitated EMT.Mechanistically,modulating S100A2 expression influenced genes associated with the Wnt/β-catenin signaling pathway.Conclusion This study reveals the significant role of S100A2 in regulating biological characteristics of OC cell line SKOV3/A2780,offering a fresh perspective for better understanding OC pathogenesis and potential therapeutic targets.