Galectin-3 regulates apoptosis and doxorubicin chemoresistance in papillary thyroid cancer cells
Galectin-3 regulates apoptosis and doxorubicin chemoresistance in papillary thyroid cancer cells
复制标题
DOI：
10.1016/j.bbrc.2008.12.153
复制
发表时间：
2009-02-06
影响因子：
3.1
通讯作者：
Ruan, Daniel T.
中科院分区：
文献类型：
--
作者：
Lin, Chi-Iou;Whang, Edward E.;Ruan, Daniel T.
甲状腺乳头状癌（PTC）患者的一个亚组表现为常规治疗难以治愈的侵袭性疾病。需要新的疗法来治疗这类患者。半乳糖凝集素-3（Gal-3）是具有抗凋亡活性的β-半乳糖苷结合蛋白。在过去的3年中，超过30项研究报道了相对于正常甲状腺细胞，Gal-3在PTC中高表达。在这项研究中，我们表明，半乳糖苷-3沉默与RNA干扰刺激细胞凋亡，而半乳糖苷-3过表达保护对TRAIL和阿霉素诱导的PTC细胞凋亡。与Gal-3功能相关的抗凋亡活性和化学抗性可以通过抑制PI 3 K-Akt途径部分逆转，表明Gal-3至少部分作用于PI 3 K-Akt轴。这些观察结果支持进一步评价Gal-3作为侵袭性PTC患者的潜在治疗靶点。(C)2008年爱思唯尔公司All rights reserved.
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.