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Down-regulation of the ErbB3 binding protein 1 in human bladder cancer promotes tumor progression and cell proliferation.

Authors :
He HC
Ling XH
Zhu JG
Fu X
Han ZD
Liang YX
Deng YH
Lin ZY
Chen G
Chen YF
Mo RJ
Zhong WD
Source :
Molecular biology reports [Mol Biol Rep] 2013 May; Vol. 40 (5), pp. 3799-805. Date of Electronic Publication: 2013 Jan 03.
Publication Year :
2013

Abstract

The ErbB3 binding protein 1 (Ebp1) represents a downstream effector of the ErbB signaling network and has been demonstrated to be a potent tumor suppressor in various human malignancies, however, its involvement in human bladder cancer is still unclear.To investigate the clinical significance and potential role of ErbB3 binding protein 1 (Ebp1) in bladder cancer. Ebp1 expression at protein and gene levels in 52 surgically removed bladder cancer specimens as well as 21 adjacent normal bladder specimens were respectively detected by immunohistochemistry and qRT-PCR. The association of Ebp1 protein expression with the clinicopathological features of bladder cancer was also statistically analyzed. Its roles in bladder cancer cell line were further evaluated. The expression level of Ebp1 protein and gene in bladder cancer tissues was significantly lower than that in adjacent normal bladder tissues (P < 0.01). When categorized into low vs. high expression, the down-regulation of Ebp1 protein was associated with the advanced pathologic stage (P = 0.036) and the high histologic grade (P = 0.001) of patients with bladder cancer. Moreover, following the transfection of Ebp1 in bladder cancer cells, not only cell proliferation and cell invasion decreased significantly, but also the cell cycle was blocked at G0/G1 stage. Our data suggest for the first time that the down-regulation of Ebp1 closely correlates with advanced clinicopathological characteristics of human bladder cancer. Furthermore, Ebp1 plays an important role in the bladder cancer cells' proliferation by regulating the cancer cell cycle from G0/G1 to S.

Details

Language :
English
ISSN :
1573-4978
Volume :
40
Issue :
5
Database :
MEDLINE
Journal :
Molecular biology reports
Publication Type :
Academic Journal
Accession number :
23283744
Full Text :
https://doi.org/10.1007/s11033-012-2458-2