Role of GSK-3β in Regulation of Canonical Wnt/β-catenin Signaling and PI3-K/Akt Oncogenic Pathway in Colon Cancer

被引：54
作者：
Jain, Shelly [1 ]
Ghanghas, Preety [1 ]
Rana, Chandan [1 ]
Sanyal, S. N. [1 ]
机构：
[1] Panjab Univ, Dept Biophys, Chandigarh 160014, India
来源：
CANCER INVESTIGATION | 2017年 / 35卷 / 07期
关键词：
Akt; beta-catenin; colorectal cancer; DMH; GSK-3; beta; PI3-K; NITRIC-OXIDE SYNTHASE; ABERRANT CRYPT FOCI; BETA-CATENIN; PHOSPHATIDYLINOSITOL; 3-KINASE/AKT; CYCLOOXYGENASE-2; INHIBITOR; COLORECTAL-CANCER; DOWN-REGULATION; APOPTOSIS; CELECOXIB; DICLOFENAC;
D O I：
10.1080/07357907.2017.1337783
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Non-steroidal anti-inflammatory drugs (NSAIDs) are emerging as novel chemopreventive agents because of their ability in blocking cellular proliferation, and thereby tumor development, and also by promoting apoptosis. GSK-3 beta, a serine threonine kinase and a negative regulator of the oncogenic Wnt/beta-catenin signaling pathway, plays a critical role in the regulation of oncogenesis. Celecoxib and etoricoxib, the two cyclooxygenase-2 (COX-2) selective NSAIDs, and Diclofenac, a preferential COX-2 inhibitory NSAID, had shown uniformly the chemopreventive and anti-neoplastic effects in the early stage of colon cancer by promoting apoptosis as well as an over-expression of GSK-3 beta while down-regulating the PI3-K/Akt oncogenic pathway.
引用
收藏
页码：473 / 483
页数：11
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