Yang Mai-Qing, Bai Lin-Lin, Wang Zhao, Lei Lei, Zheng Yi-Wen, Li Zhi-Han, Huang Wen-Jing, Liu Chen-Chen, Xu Hong-Tao
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, Changyi People's Hospital, Changyi, Shandong 261300, P.R. China.
Oncol Lett. 2021 Jun;21(6):440. doi: 10.3892/ol.2021.12701. Epub 2021 Apr 1.
DEK proto-oncogene (DEK) has been demonstrated as an oncogene and is associated with the development of many types of tumor; however, the expression and role of DEK in breast cancer remain unknown. The present study aimed to determine the role of DEK in the progression of breast cancer. The expression of DEK in 110 breast cancer tissues and 50 adjacent normal breast tissues was examined using immunohistochemistry. Furthermore, DEK expression was upregulated by DEK transfection or downregulated by DEK shRNA interference in MCF7 cells. Proliferative and invasive abilities were examined in MCF7 cells using MTT assay, colony-formation assay and transwell invasion assays. The results demonstrated that DEK expression level was significantly increased in breast cancer tissues compared with normal breast tissues. Furthermore, high DEK expression was associated with high histological grade, lymph node metastasis, advanced Tumor-Node-Metastasis stage and high Ki-67 index; however, DEK expression was not associated with the expression level of estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2. High DEK expression indicated poor prognosis in patients with breast cancer. DEK overexpression upregulated the protein expression of β-catenin and Wnt and increased the proliferative and invasive abilities of breast cancer cells. DEK downregulation had the opposite effect. Taken together, the results from the present study demonstrated that high expression of DEK was common in patients with breast cancer and was associated with progression of the disease and poor prognosis, and that DEK overexpression promoted the proliferative and invasive abilities of breast cancer cells.
DEK原癌基因（DEK）已被证明是一种癌基因，与多种肿瘤的发生发展相关；然而，DEK在乳腺癌中的表达及作用仍不清楚。本研究旨在确定DEK在乳腺癌进展中的作用。采用免疫组织化学法检测110例乳腺癌组织和50例癌旁正常乳腺组织中DEK的表达。此外，通过DEK转染上调MCF7细胞中DEK的表达，或通过DEK shRNA干扰下调其表达。采用MTT法、集落形成试验和Transwell侵袭试验检测MCF7细胞的增殖和侵袭能力。结果表明，与正常乳腺组织相比，乳腺癌组织中DEK表达水平显著升高。此外，DEK高表达与高组织学分级、淋巴结转移、晚期肿瘤-淋巴结-转移分期及高Ki-67指数相关；然而，DEK表达与雌激素受体、孕激素受体和人表皮生长因子受体2的表达水平无关。DEK高表达提示乳腺癌患者预后不良。DEK过表达上调β-连环蛋白和Wnt的蛋白表达，增加乳腺癌细胞的增殖和侵袭能力。DEK下调则产生相反的效果。综上所述，本研究结果表明，DEK高表达在乳腺癌患者中常见，与疾病进展和预后不良相关，且DEK过表达促进乳腺癌细胞的增殖和侵袭能力。
