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Tumor suppressor function of BCSC-1 in nasopharyngeal carcinoma.

Authors :
Zhou, Y. Q.
Chen, S. L.
Ju, J. Y.
Shen, L.
Liu, Y.
Zhen, S.
Lv, N.
He, Z. G.
Zhu, L. P.
Source :
Cancer Science; Oct2009, Vol. 100 Issue 10, p1817-1822, 6p, 5 Graphs
Publication Year :
2009

Abstract

BCSC-1 is dramatically upregulated in CNE-2L2 human nasopharyngeal carcinoma cells with reduced malignancy (AS cells) and is proposed to be a candidate tumor suppressor gene. We therefore examined the effect of BCSC-1 expression on malignant behaviors of CNE-2L2 cells. Growth in vitro and tumorigenesis in nude mice of wild-type CNE-2L2 cells (W cells) were inhibited by ectopic BCSC-1, and those of AS cells were promoted by BCSC-1 suppression. The tumor suppressor function of BCSC-1 was further confirmed by a study showing that intratumor BCSC-1 injection caused growth suppression of the tumor from W cells inoculated in nude mice. Immunohistochemistry exhibited marked reduction of BCSC-1 expression in 11 of 39 human nasopharyngeal carcinoma specimens. Because BCSC-1 expression was as rich as that in normal cells in the rest of the carcinoma specimens and was poor in CNE-2L2 cells, HNE-1 human nasopharyngeal carcinoma cells with rich BCSC-1 expression were used as a control in the study. No effect of BCSC-1 transfection on growth of the cells was observed. The data suggest that BCSC-1 suppression might play roles in tumorigenesis of some nasopharyngeal carcinomas and that BCSC-1 might be a potential gene therapy target in nasopharyngeal carcinomas with poor BCSC-1 expression. Enhanced aggregation of cells together with increased E-cadherin and α-catenin expression and reduced Wnt signaling might be involved in the mechanisms of tumor suppressor function of BCSC-1. ( Cancer Sci 2009; 100: 1817–1822) [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
13479032
Volume :
100
Issue :
10
Database :
Complementary Index
Journal :
Cancer Science
Publication Type :
Academic Journal
Accession number :
44183021
Full Text :
https://doi.org/10.1111/j.1349-7006.2009.01261.x