Galectin-3 regulates apoptosis and doxorubicin chemoresistance in papillary thyroid cancer cells

被引：44

作者：

Lin, Chi-Iou ^{[1
]}

Whang, Edward E. ^{[1
]}

Abramson, Michael A. ^{[1
]}

Donner, David B. ^{[2
]}

Bertagnolli, Monica M. ^{[1
]}

Moore, Francis D., Jr. ^{[1
]}

Ruan, Daniel T. ^{[1
]}

机构：

[1] Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA

[2] Univ Calif San Francisco, Dept Surg, San Francisco, CA 94115 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2009年 / 379卷 / 02期

关键词：

Galectin-3; Papillary thyroid cancer; Doxorubicin chemoresistance; FOLLICULAR VARIANT; CARCINOMA; IDENTIFICATION; EXPRESSION; AKT; OVEREXPRESSION; INHIBITION; PROTECTS; ADHESION; CATENIN;

D O I：

10.1016/j.bbrc.2008.12.153

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

A Subset of patients with papillary thyroid cancer (PTC) present with aggressive disease that is refractory to conventional treatment. Novel therapies are needed to treat this group of patients. Galectin-3 (Gal-3) is a beta-galactoside-binding protein with anti-apoptotic activity. Over 30 studies in the last 3 years have reported that Gal-3 is highly expressed in PTC relative to normal thyrocytes. In this study, we show that Gal-3 silencing with RNA interference Stimulates apoptosis, while Gal-3 overexpression protects against both TRAIL- and doxorubicin-induced apoptosis in PTC cells. The anti-apoptotic activity and chemoresistance related to Gal-3 function can be partially reversed through the inhibition of the PI3K-Akt pathway, Suggesting that Gal-3 acts, at least in part, on the PI3K-Akt axis. These observations Support further evaluation of Gal-3 as a potential therapeutic target in patients with aggressive PTC. (C) 2008 Elsevier Inc. All rights reserved.

引用

页码：626 / 631

页数：6

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