Ward 2, Department of Cardiothoracic Surgery, The Third Affiliated Hospital of Qiqihar Medical College, No. 27, Taishun Street, Tiefeng District, Qiqihar, 161000, Heilongjiang Province, China.
World J Surg Oncol. 2021 Aug 16;19(1):242. doi: 10.1186/s12957-021-02362-8.
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.
为了研究 EFNA1 在广谱肿瘤中的表达及临床意义,并评估其与食管癌(ESCA)患者预后和生物学功能的关系。
根据 TCGA 数据库中的数据,分析 EFNA1 在各种癌症中的表达情况。整合临床资料,分析与 ESCA 临床参数及预后的关系,并采用免疫组化(IHC)检测 ESCA 组织标本中 EFNA1 的表达。基于生物信息学,分析 EFNA1 过表达的功能背景。通过 EFNA1-shRNA 转染 ESCA 细胞,建立 EFNA1 敲低细胞模型,通过 MTT 检测敲低 EFNA1 对 ESCA 细胞增殖的影响。
在 TCGA 的 7563 例样本中,EFNA1 基因在 15 例常见癌症中高表达,且危及肿瘤患者的预后。EFNA1 在 ESCA 中的高表达及其对预后的影响最为显著。采用 IHC 检测 80 例 ESCA 患者及其配对样本中 EFNA1 的表达,验证其在 ESCA 组织中的高表达(配对 t 检验,P<0.001)。发现 EFNA1 的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 是独立的危险因素。为了进一步探讨 EFNA1 在肿瘤中的重要性,从 8 种 ESCA 相关细胞系中筛选 EC-9706 和 ECA109 细胞,构建 EFNA1 敲低细胞模型。结果表明,EFNA1 敲低显著抑制肿瘤细胞的增殖(P<0.05)。在分子机制方面,根据通路富集分析,EFNA1 相关基因在增殖通路上显著富集。基于细胞实验发现,敲低 EFNA1 确实抑制了细胞增殖。
EFNA1 在 ESCA 组织中的过表达与患者的预后有关。敲低 EFNA1 可显著抑制 ESCA 细胞的增殖。