Department of Pathology, The First Hospital and College of Basic Medical Sciences of China Medical University, Shenyang, Liaoning 110001, P.R. China.
Department of Pathology, Shenyang 242 Hospital, Shenyang, Liaoning 110001, P.R. China.
Oncol Rep. 2020 Apr;43(4):1338-1348. doi: 10.3892/or.2020.7488. Epub 2020 Feb 3.
DEK has been revealed to be overexpressed in many cancers and associated with cancer progression. The aim of the present study was to elucidate the role of DEK with a specific focus on its underlying mechanism in lung cancers. DEK expression in lung cancers and normal lung tissues and the correlations between DEK expression and clinicopathological parameters of lung cancers were investigated using the data from The Cancer Genome Atlas (TCGA). DEK expression was upregulated by DEK transfection or downregulated by DEK shRNA interference in A549 and H1299 cells. The effects of DEK on the Wnt signaling pathway and epithelial‑mesenchymal transition (EMT) were examined using western blotting. Proliferative and invasive abilities were observed in A549 and H1299 cells treated with DEK using an MTT assay, colony formation assay, and Transwell migration and invasion assays. The expression of DEK was higher in lung cancer tissues than that in normal lung tissues. DEK expression was positively correlated with the expression of epidermal growth factor receptor (EGFR) and KRAS in lung adenocarcinomas. High expression of DEK indicated poor prognosis in lung adenocarcinomas (P=0.018). Enhanced expression of DEK upregulated the levels of active‑β‑catenin and Wnt target genes, such as cyclin D1, c‑Myc and MMP7 and increased the proliferative and invasive abilities of lung cancer cells. Enhanced expression of DEK in A549 and H1299 cells also increased the levels of EGFR, KRAS, vimentin, Snail, and N‑cadherin, and decreased the level of E‑cadherin. The opposite results were obtained with knockdown of DEK expression. DEK was highly expressed in lung cancers and indicated poor prognosis in lung adenocarcinomas. DEK expression activated the Wnt signaling pathway and EMT process and promoted the proliferation and invasion of lung cancers.
DEK 在许多癌症中过表达，并与癌症进展相关。本研究旨在阐明 DEK 的作用，特别关注其在肺癌中的潜在机制。使用来自癌症基因组图谱 (TCGA) 的数据，研究了 DEK 在肺癌和正常肺组织中的表达以及 DEK 表达与肺癌临床病理参数之间的相关性。通过 DEK 转染上调 DEK 表达或通过 DEK shRNA 干扰下调 DEK 表达，在 A549 和 H1299 细胞中。使用 Western blot 检测 DEK 对 Wnt 信号通路和上皮-间充质转化 (EMT) 的影响。通过 MTT 测定、集落形成测定和 Transwell 迁移和侵袭测定观察 DEK 处理对 A549 和 H1299 细胞增殖和侵袭能力的影响。肺癌组织中 DEK 的表达高于正常肺组织。在肺腺癌中，DEK 表达与表皮生长因子受体 (EGFR) 和 KRAS 的表达呈正相关。DEK 高表达表明肺腺癌预后不良 (P=0.018)。增强的 DEK 表达上调了活性-β-连环蛋白和 Wnt 靶基因的水平，如细胞周期蛋白 D1、c-Myc 和 MMP7，并增加了肺癌细胞的增殖和侵袭能力。在 A549 和 H1299 细胞中增强 DEK 的表达也增加了 EGFR、KRAS、波形蛋白、Snail 和 N-钙粘蛋白的水平，并降低了 E-钙粘蛋白的水平。DEK 表达下调则得到相反的结果。DEK 在肺癌中高表达，在肺腺癌中预示预后不良。DEK 表达激活了 Wnt 信号通路和 EMT 过程，促进了肺癌的增殖和侵袭。
