Li Xiang, Huang Jiepeng, Yu Tingting, Fang Xiaoting, Lou Liqin, Xin Shijun, Ji Ling, Jiang Feizhao, Lou Yongliang
Wenzhou Key Laboratory of Sanitary Microbiology, Key Laboratory of Laboratory Medicine, Ministry of Education, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, China.
Colorectal Cancer Research Center, Wenzhou Medical University, Wenzhou, China.
Front Microbiol. 2021 Jan 6;11:545251. doi: 10.3389/fmicb.2020.545251. eCollection 2020.
BACKGROUND/AIMS: Growing evidence supports the direct link of with colorectal cancer (CRC). However, to date, the underlying mechanism of action remains poorly understood. In this study, we examined the effects of on the progression of CRC and investigated whether cyclin-dependent kinase 5 (Cdk5) is involved in the effect through activating the Wnt/β-catenin signaling pathway.
CRC tissues and matched histologically normal specimens were collected from patients who were diagnosed with CRC and underwent surgical treatment in our hospital between January 2018 and January 2019. Two human CRC cell lines, including DLD-1 and SW480, were utilized mainly for mechanistic investigations.
The abundance of was significantly greater in CRC tissues than in cancer-free specimens, which was significantly correlated with the progression of CRC. investigations revealed that significantly enhanced the proliferation and migration of CRC cells. Furthermore, significantly induced the expression of Cdk5 and activation of the Wnt/β-catenin signaling pathway. Notably, knockdown of Cdk5 significantly abrogated the effects of on cellular processes and Wnt/β-catenin signaling in relation to the progression of CRC.
The results of this study demonstrate that orchestrates a molecular network involving the direct role of Cdk5 in activating Wnt/β-catenin signaling to modulate CRC progression. Thus, in-depth investigations of associated molecular pathways may offer valuable insight into the pathogenesis of CRC, which may help further the development of treatment for this disease.
背景/目的：越来越多的证据支持[具体物质]与结直肠癌（CRC）之间的直接联系。然而，迄今为止，其潜在的作用机制仍知之甚少。在本研究中，我们检测了[具体物质]对CRC进展的影响，并研究细胞周期蛋白依赖性激酶5（Cdk5）是否通过激活Wnt/β-连环蛋白信号通路参与该效应。
收集2018年1月至2019年1月期间在我院被诊断为CRC并接受手术治疗的患者的CRC组织及组织学上匹配的正常标本。主要利用两种人CRC细胞系，即DLD-1和SW480进行[具体物质]的机制研究。
CRC组织中[具体物质]的丰度显著高于癌旁标本，且与CRC的进展显著相关。[具体物质]研究表明，[具体物质]显著增强了CRC细胞的增殖和迁移。此外，[具体物质]显著诱导Cdk5的表达并激活Wnt/β-连环蛋白信号通路。值得注意的是，敲低Cdk5显著消除了[具体物质]对CRC进展相关细胞过程和Wnt/β-连环蛋白信号的影响。
本研究结果表明，[具体物质]协调了一个分子网络，其中Cdk5直接参与激活Wnt/β-连环蛋白信号以调节CRC进展。因此，对相关分子途径的深入研究可能为CRC的发病机制提供有价值的见解，这可能有助于推动该疾病治疗方法的进一步发展。
