食管癌（EC）是一种恶性肿瘤，在全世界范围内导致大量癌症相关死亡。 EC发病机制的分子机制尚未完全阐明。来自基因表达综合数据库（GEO）的GSE17351和GSE20347数据集被用来筛选差异表达基因（DEG）。逆转录定量PCR (RT-qPCR) 用于检测hub 基因表达。使用编码GABRP的pcDNA3.1表达载体转染ECA-109和TE-12细胞。进行细胞计数试剂盒8（CCK-8）、细胞划痕和Transwell实验来评估GABRP对EC细胞增殖、迁移和侵袭的影响。通过蛋白质印迹法测量上皮间质转化（EMT）相关蛋白水平。随后，CFTR被敲低，以验证GABRP是否通过靶向CFTR影响EC细胞中的生物学事件。鉴定出 7 个中心基因，包括 GABRP、FLG、ENAH、KLF4、CD24、ABLIM3 和 ABLIM1，它们都可以用作 EC 的诊断生物标志物。 RT-qPCR结果表明，GABRP、FLG、KLF4、CD24、ABLIM3和ABLIM1的表达水平下调，而ENAH的表达水平上调。体外功能测定表明，GABRP 过表达可抑制 EC 细胞的增殖、迁移、侵袭和 EMT。从机制上讲，GABRP 促进 CFTR 的表达，CFTR 敲低显着抵消了 GABRP 过表达对 EC 细胞生物学事件的影响。 GABRP 的过表达通过增加 CFTR 表达来抑制 EC 进展，这可能成为 EC 治疗的新靶点。© 2024 Company of the International Journal of Experimental Pathology (CIJEP)。

Oesophageal cancer (EC) is a malignancy which accounts for a substantial number of cancer-related deaths worldwide. The molecular mechanisms underlying the pathogenesis of EC have not been fully elucidated. GSE17351 and GSE20347 data sets from the Gene Expression Omnibus (GEO) database were employed to screen differentially expressed genes (DEGs). Reverse transcription quantitative PCR (RT-qPCR) was used to examine hub gene expression. ECA-109 and TE-12 cells were transfected using the pcDNA3.1 expression vector encoding GABRP. The cell counting kit-8 (CCK-8), cell scratch and Transwell assays were performed to assess the effect of GABRP on EC cell proliferation, migration and invasion. Epithelial-mesenchymal transition (EMT)-associated protein levels were measured by Western blotting. Subsequently, CFTR was knocked down to verify whether GABRP affected biological events in EC cells by targeting CFTR. Seven hub genes were identified, including GABRP, FLG, ENAH, KLF4, CD24, ABLIM3 and ABLIM1, which all could be used as diagnostic biomarkers for EC. The RT-qPCR results indicated that the expression levels of GABRP, FLG, KLF4, CD24, ABLIM3 and ABLIM1 were downregulated, whereas the expression level of ENAH was upregulated. In vitro functional assays demonstrated that GABRP overexpression suppressed the proliferation, migration, invasion and EMT of EC cells. Mechanistically, GABRP promoted the expression of CFTR, and CFTR knockdown significantly counteracted the influence of GABRP overexpression on biological events in EC cells. Overexpression of GABRP inhibited EC progression by increasing CFTR expression, which might be a new target for EC treatment.© 2024 Company of the International Journal of Experimental Pathology (CIJEP).