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附睾蛋白3A在非小细胞肺癌中上调并促进细胞增殖。

Epididymal protein 3A is upregulated and promotes cell proliferation in non-small cell lung cancer.

作者信息

Li Guangbin, Tong Xing, Pan Liangbin, Huang Haitao, Ma Haitao, Feng Yu

机构信息

Department of Thoracic Surgery, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215000, P.R. China.

Department of Pathology, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215000, P.R. China.

出版信息

Oncol Lett. 2020 Jun;19(6):4024-4030. doi: 10.3892/ol.2020.11517. Epub 2020 Apr 7.

Abstract

Lung cancer is one of the most common cancer types and a major contributor to cancer-associated mortalities worldwide. The aim of the present study was to investigate the function of the epididymal protein 3A (EDDM3A) in non-small cell lung cancer (NSCLC). Data from patients with NSCLC were retrieved from The Cancer Genome Atlas and analyzed, and the differences in EDDM3A expression level between 30 NSCLC tissues and matched adjacent non-tumor tissues (>5 cm) were assessed via tissue microarray analysis. It was revealed that, compared with adjacent non-tumor tissues, EDDM3A expression was significantly increased in NSCLC tissues (P=4.19×10). To knock down EDDM3A expression in a human NSCLC cell line, lentivirus-mediated short hairpin RNAs (shRNAs) were used, and the knockdown efficiency was assessed via reverse transcription-quantitative PCR and western blotting. Moreover, cell proliferation was evaluated with an MTT assay and Celigo imaging cytometry. In addition, cell apoptosis was detected by Annexin V staining. It was demonstrated that knockdown of EDDM3A inhibited the proliferation of A549 cells. Furthermore, compared with the control group, the apoptotic rate of the EDDM3A-shRNA group was significantly higher. Collectively, the present results indicate the potential role of EDDM3A in NSCL and suggest that EDDM3A may represent a potent therapeutic target for treating patients with NSCLC.

摘要

肺癌是最常见的癌症类型之一,也是全球癌症相关死亡率的主要促成因素。本研究的目的是探讨附睾蛋白3A(EDDM3A)在非小细胞肺癌(NSCLC)中的作用。从癌症基因组图谱中检索并分析非小细胞肺癌患者的数据,并通过组织芯片分析评估30例非小细胞肺癌组织与匹配的相邻非肿瘤组织(>5 cm)之间EDDM3A表达水平的差异。结果显示,与相邻非肿瘤组织相比,非小细胞肺癌组织中EDDM3A表达显著增加(P=4.19×10)。为了在人非小细胞肺癌细胞系中敲低EDDM3A表达,使用了慢病毒介导的短发夹RNA(shRNA),并通过逆转录定量PCR和蛋白质印迹法评估敲低效率。此外,用MTT法和Celigo成像细胞仪评估细胞增殖。另外,通过膜联蛋白V染色检测细胞凋亡。结果表明,敲低EDDM3A可抑制A549细胞的增殖。此外,与对照组相比,EDDM3A-shRNA组的凋亡率显著更高。总体而言,本研究结果表明EDDM3A在非小细胞肺癌中的潜在作用,并提示EDDM3A可能是治疗非小细胞肺癌患者的有效治疗靶点。

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