BRE enhances in vivo growth of tumor cells

被引:18
作者
Chan, BCL
Li, Q
Chow, SKY
Ching, AKK
Liew, CT
Lim, PL
Lee, KKH
Chan, JYH
Chui, YL [1 ]
机构
[1] Chinese Univ Hong Kong, Prince Wales Hosp, Clin Immunol Unit, Shatin, Hong Kong, Peoples R China
[2] Chinese Univ Hong Kong, Prince Wales Hosp, Sir YK Pao Ctr Canc, Shatin, Hong Kong, Peoples R China
[3] Chinese Univ Hong Kong, Prince Wales Hosp, Dept Anat & Cellular Pathol, Shatin, Hong Kong, Peoples R China
[4] Chinese Univ Hong Kong, Dept Anat, Shatin, Hong Kong, Peoples R China
[5] Univ Texas, MD Anderson Canc Ctr, Dept Mol Pathol, Houston, TX 77030 USA
关键词
BRE; apoptosis; antiapoptotic protein; cancer; Lewis lung carcinoma; D122; tumorigenesis; metastasis; death receptor-associating protein; TNF-alpha;
D O I
10.1016/j.bbrc.2004.11.013
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
Human BRE, a death receptor-associating intracellular protein, attenuates apoptotic response of human and mouse tumor cell lines to death receptor stimuli in vitro. In this report, we addressed whether the in vitro antiapoptotic effect of BRE could impact on tumor growth in vivo. We have shown that the mouse Lewis lung carcinoma D122 stable transfectants of human BRE expression vector developed into local tumor significantly faster than the stable transfectants of empty vector and parental D122, in both the syngeneic C57BL/6 host and nude mice. In vitro growth of the BRE stable transfectants was, however, not accelerated. No significant difference in metastasis between the transfectants and the parental D122 was detected. Thus, overexpression of BRE promotes local tumor growth but not metastasis. We conclude that the enhanced tumor growth is more likely due to the antiapoptotic activity of BRE than any direct effect of the protein on cell proliferation. (C) 2004 Published by Elsevier Inc.
引用
收藏
页码:268 / 273
页数:6
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