To investigate the expression and clinical significance of EFNA1 in broad-spectrum tumors, and to evaluate its relationship with prognosis and biological functions of esophageal carcinoma (ESCA). EFNA1 expression in various cancers was analyzed according to the data in the TCGA database. The clinical data were integrated, to analyze the relationship with ESCA clinical parameters and prognosis, and EFNA1 expression in ESCA tissue samples was detected by immunohistochemistry (IHC). Based on bioinformatics, the functional background of EFNA1 overexpression was analyzed. EFNA1 knockout cell model was established by EFNA1-shRNA transfecting ESCA cells, and the effect of knocking down EFNA1 on the proliferation of ESCA cells was detected by MTT. Among 7563 samples from TCGA, the EFNA1 gene highly expressed in 15 samples with common cancers and endangered the prognosis of patients with tumors. Its overexpression in ESCA and its influence on the prognosis were most significant. EFNA1 expression in 80 samples with ESCA and their paired samples was tested by IHC to verify its high expression (paired t test, P < 0.001) in ESCA tissues. It was found that EFNA1 expression was related to clinical factors (TNM staging, P = 0.031; lymph node metastasis, P = 0.043; infiltration, P = 0.016). Meanwhile, EFNA1 was found to be an independent risk factor based on the COX multi-factor analysis. And to further explore the importance of EFNA1 in tumors, EC-9706 and ECA109 cells were screened from 8 ESCA-related cell lines to build EFNA1 knockdown cell models. The results showed that EFNA1 knockdown significantly inhibited the proliferation of tumor cells (P < 0.05). In terms of molecular mechanism, EFNA1 related genes were significantly enriched in the proliferative pathway according to the pathway enrichment analysis. It was found that knocking down EFNA1 did inhibit cell proliferation based on cell experiments. EFNA1 overexpression in ESCA tissue is related to the prognosis of patients. Knocking down EFNA1 can significantly inhibit the proliferation of ESCA cells.

中文翻译：

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EFNA1对食管癌细胞表型及预后的影响

探讨EFNA1在广谱肿瘤中的表达及临床意义，评价其与食管癌（ESCA）预后及生物学功能的关系。根据TCGA数据库中的数据分析各种癌症中EFNA1的表达。整合临床资料，分析与ESCA临床参数及预后的关系，并采用免疫组织化学（IHC）检测ESCA组织样本中EFNA1的表达。基于生物信息学，分析了EFNA1过表达的功能背景。EFNA1-shRNA转染ESCA细胞建立EFNA1敲除细胞模型，MTT检测敲低EFNA1对ESCA细胞增殖的影响。在来自 TCGA 的 7563 个样本中，EFNA1基因在15例常见癌症样本中高表达，危及肿瘤患者的预后。其在ESCA中的过度表达及其对预后的影响最为显着。EFNA1 在 80 个 ESCA 样本及其配对样本中的表达通过 IHC 进行测试，以验证其在 ESCA 组织中的高表达（配对 t 检验，P < 0.001）。发现EFNA1表达与临床因素有关（TNM分期，P=0.031；淋巴结转移，P=0.043；浸润，P=0.016）。同时，基于 COX 多因素分析发现 EFNA1 是一个独立的危险因素。为了进一步探索EFNA1在肿瘤中的重要性，从8个ESCA相关细胞系中筛选出EC-9706和ECA109细胞，构建EFNA1敲低细胞模型。结果显示EFNA1敲低显着抑制肿瘤细胞的增殖（P < 0.05）。在分子机制方面，通过通路富集分析，EFNA1相关基因在增殖通路中显着富集。根据细胞实验发现，敲低EFNA1确实抑制了细胞增殖。ESCA组织中EFNA1的过表达与患者的预后有关。敲低EFNA1可显着抑制ESCA细胞的增殖。ESCA组织中EFNA1的过表达与患者的预后有关。敲低EFNA1可显着抑制ESCA细胞的增殖。ESCA组织中EFNA1的过表达与患者的预后有关。敲低EFNA1可显着抑制ESCA细胞的增殖。