Inhibition of cell transformation by sulindac sulfide is confined to specific oncogenic pathways

被引：13

作者：

Gala, M

Sun, RG

Yang, VW

机构：

[1] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA

[2] Johns Hopkins Univ, Sch Med, Dept Biol Chem, Baltimore, MD 21205 USA

[3] Johns Hopkins Univ, Sch Med, Johns Hopkins Oncol Ctr, Baltimore, MD 21205 USA

来源：

CANCER LETTERS | 2002年 / 175卷 / 01期

关键词：

chemoprevention; non-steroidal anti-inflammatory drugs; oncogene; Ha-Ras; v-Src; G alpha 12; G alpha 13; focus formation assay; transformation;

D O I：

10.1016/S0304-3835(01)00716-9

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Non-steroidal anti-inflammatory drugs (NSAIDs) have been shown to reduce the risk of colorectal cancer (CRC). They are also known to induce the regression of colorectal adenomas, which are precursors to CRC. Despite these evidences, the exact mechanism by which NSAIDs exerts its anti-oncogenic effect is not completely understood. Using a focus formation assay, here we show that sulindac sulfide, a NSAID, specifically inhibits cell transformation mediated by oncogenic Ha-Ras, but not by other established oncogene products such as v-Src, Galpha12, and Galpha13. Our results suggest that the ability of sulindac sulfide to suppress transformation is confined to specific oncogenic pathways. Further studies of the sulindac-resistant oncogenic pathways may lead to identification of novel therapeutic agents that are effective in the prevention or treatment of CRC. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：89 / 94

页数：6

共 35 条

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