CDC42EP3通过调节细胞增殖、细胞凋亡和细胞迁移来促进结直肠癌。
CDC42EP3 promotes colorectal cancer through regulating cell proliferation, cell apoptosis and cell migration.
作者信息
Feng Qiang, Xu Dongkui, Zhou Mingyao, Wu Zijian, Wu Zhiyuan, Wang Zheng, Bi Jianjun, Pei Wei
机构信息
Department of Colorectal Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Department of VIP, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
出版信息
Cancer Cell Int. 2021 Mar 16;21(1):169. doi: 10.1186/s12935-021-01845-8.
BACKGROUND
Nowadays, colorectal cancer (CRC) is one of the most commonly diagnosed malignant tumors worldwide, the incidence rate of which is still increasing year by year. Herein, the objective of this study is to investigate whether CDC42EP3 has regulatory effects in CRC.
METHODS
First, CDC42EP3 knockdown cell model based on HCT116 and RKO cell lines was successfully constructed, which was further used for constructing mouse xenotransplantation models. Importantly, effects of CDC42EP3 knockdown on proliferation, colony formation, apoptosis, and migration of CRC were accessed by MTT assay, EdU staining assay, colony formation assay, Flow cytometry, and Transwell assay.
RESULTS
As the results, we showed that CDC42EP3 was significantly upregulated in CRC, and its high expression was associated with tumor progression. Furthermore, knockdown of CDC42EP3 could inhibit proliferation, colony formation and migration, and promote apoptosis of CRC cells in vitro. In vivo results further confirmed knockdown of CDC42EP3 attenuated tumor growth in CRC. Interestingly, the regulation of CRC by CDC42EP3 involved not only the change of a variety of apoptosis-related proteins, but also the regulation of downstream signaling pathway.
CONCLUSION
In conclusion, the role of CDC42EP3 in CRC was clarified and showed its potential as a target of innovative therapeutic approaches for CRC.
背景
如今，结直肠癌（CRC）是全球最常被诊断出的恶性肿瘤之一，其发病率仍在逐年上升。在此，本研究的目的是探讨CDC42EP3在结直肠癌中是否具有调节作用。
方法
首先，成功构建了基于HCT116和RKO细胞系的CDC42EP3敲低细胞模型，并进一步用于构建小鼠异种移植模型。重要的是，通过MTT法、EdU染色法、集落形成试验、流式细胞术和Transwell试验评估CDC42EP3敲低对结直肠癌增殖、集落形成、凋亡和迁移的影响。
结果
结果显示，CDC42EP3在结直肠癌中显著上调，其高表达与肿瘤进展相关。此外，敲低CDC42EP3可在体外抑制结直肠癌细胞的增殖、集落形成和迁移，并促进其凋亡。体内结果进一步证实敲低CDC42EP3可减弱结直肠癌的肿瘤生长。有趣的是，CDC42EP3对结直肠癌的调节不仅涉及多种凋亡相关蛋白的变化，还涉及下游信号通路的调节。
结论
总之，阐明了CDC42EP3在结直肠癌中的作用，并显示出其作为结直肠癌创新治疗方法靶点的潜力。
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