Dysregulation and crosstalk of cellular signaling pathways in colon carcinogenesis

被引:96
作者
Wu, William K. K. [1 ,2 ]
Wang, Xiao J. [1 ,2 ]
Cheng, Alfred S. L. [1 ,2 ]
Luo, Millore X. M. [3 ]
Ng, Simon S. M. [4 ]
To, Ka F. [5 ]
Chan, Francis K. L. [1 ,2 ]
Cho, Chi H. [3 ]
Sung, Joseph J. Y. [1 ,2 ]
Yu, Jun [1 ,2 ]
机构
[1] Chinese Univ Hong Kong, LKS Inst Hlth Sci, Inst Digest Dis, Fac Med, Hong Kong, Hong Kong, Peoples R China
[2] Chinese Univ Hong Kong, Fac Med, Dept Med & Therapeut, Hong Kong, Hong Kong, Peoples R China
[3] Chinese Univ Hong Kong, Sch Biomed Sci, Fac Med, Hong Kong, Hong Kong, Peoples R China
[4] Chinese Univ Hong Kong, Div Colorectal Surg, Dept Surg, Fac Med, Hong Kong, Hong Kong, Peoples R China
[5] Chinese Univ Hong Kong, Dept Anat Cellular Pathol, Fac Med, Hong Kong, Hong Kong, Peoples R China
关键词
Colorectal cancer; Cell signaling; Wnt; p53; Ras; NF-KAPPA-B; GROWTH-FACTOR RECEPTOR; JUN NH2-TERMINAL KINASE; PROAPOPTOTIC GENE BAX; APC TUMOR-SUPPRESSOR; TGF-BETA SIGNAL; CYCLIN D1 GENE; COLORECTAL-CANCER; DOWN-REGULATION; NUCLEAR-FACTOR;
D O I
10.1016/j.critrevonc.2012.11.009
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Multiple intracellular signaling pathways, such as Wnt/beta-catenin signaling, epidermal growth factor receptor/Ras signaling, and p53 signaling are frequently dysregulated in colorectal cancer. Recent evidence also points to the involvement of signaling pathways in the developmental process, including Notch signaling, Hedgehog signaling, and Hippo signaling. Dysregulation of these signaling pathways contribute to the acquisition of malignant phenotypes, including unchecked cell cycle progression, evasion of apoptosis, induction of genetic instability, and enhanced invasiveness and metastasis. Understanding their relative importance and crosstalk will provide a rational basis for anticancer drug development. (c) 2012 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:251 / 277
页数:27
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