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

页码：473 / 483

页数：11

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