Mechanisms underlying cancer growth and apoptosis by DEK overexpression in colorectal cancer.
Mechanisms underlying cancer growth and apoptosis by DEK overexpression in colorectal cancer.
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DEK 在结直肠癌中过度表达导致癌症生长和细胞凋亡的机制
DOI：
10.1371/journal.pone.0111260
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Lin Z
中科院分区：
文献类型：
--
作者：
Lin L;Piao J;Ma Y;Jin T;Quan C;Kong J;Li Y;Lin Z
我们先前的研究表明，与正常大肠粘膜相比，结直肠癌组织中DEK蛋白过表达。DEK还与结直肠癌患者的预后特征显著相关，表明DEK在结直肠癌的进展中起重要作用。在这项工作中，我们评估了DEK对结直肠癌生物学行为的影响，并探索了相关的分子机制。结果表明，DEK在人结直肠癌组织中高表达，并与Ki-67指数和细胞凋亡指数呈正相关。Sw-620和HCT116细胞中的DEK被RNAi耗尽后，细胞增殖显著降低，但细胞凋亡率增加。DEK表达上调涉及P53/MDM、Bcl2家族和caspase通路。我们的研究表明，DEK促进了结直肠癌的生长，并可能成为结直肠癌的治疗靶点。
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.
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