Lin Lijuan, Piao Junjie, Ma Yibing, Jin Tiefeng, Quan Chengshi, Kong Jienan, Li Yulin, Lin Zhenhua
Department of Pathology & Cancer Research Center, Yanbian University Medical College, Yanji, China; Department of Medical Imaging, College of Medicine, Eastern Liaoning University, Dandong, China.
Department of Pathology & Cancer Research Center, Yanbian University Medical College, Yanji, China.
PLoS One. 2014 Oct 23;9(10):e111260. doi: 10.1371/journal.pone.0111260. eCollection 2014.
Our previous study indicated that DEK protein was overexpressed in colorectal carcinoma (CRC) compared with the normal colorectal mucosa. DEK was also significantly correlated with the prognostic characteristics of patients with CRC, demonstrating that DEK played an important role in CRC progression. In this work, we evaluate the effects of DEK on biological behaviors in CRC and explore the related molecular mechanisms. The results showed that DEK was overexpressed in human CRC tissues, and was correlated with the Ki-67 index and the apoptotic index. DEK depletion by RNAi in SW-620 and HCT116 cells significantly decreased cell proliferation, but increased cell apoptosis. Upregulation of DEK was involved in the p53/MDM, Bcl-2 family, and caspase pathways. Our study demonstrates that DEK promotes the growth of CRC, and could be a therapeutic target in CRC.
我们之前的研究表明，与正常结直肠黏膜相比，DEK蛋白在结直肠癌（CRC）中过表达。DEK也与CRC患者的预后特征显著相关，表明DEK在CRC进展中起重要作用。在这项工作中，我们评估了DEK对CRC生物学行为的影响，并探索相关分子机制。结果显示，DEK在人CRC组织中过表达，且与Ki-67指数和凋亡指数相关。在SW-620和HCT116细胞中通过RNAi敲低DEK可显著降低细胞增殖，但增加细胞凋亡。DEK的上调涉及p53/MDM、Bcl-2家族和半胱天冬酶途径。我们的研究表明，DEK促进CRC生长，可能是CRC的一个治疗靶点。
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