ALKBH8 promotes bladder cancer growth and progression through regulating the expression of survivin.

Abstract:

:Human AlkB homolog 8 (ALKBH8) is highly expressed in high-grade, superficially and deeply invasive bladder cancer. Moreover, ALKBH8 knockdown induces apoptosis in bladder cancer cells. However, the underlying anti-apoptotic mechanism of ALKBH8 in bladder cancer cells has thus far remained unclear. Moreover, there is no direct evidence that highly expressed ALKBH8 is involved in tumor progression in vivo. We here show that ALKBH8 knockdown induced apoptosis via downregulating the protein expression of survivin, an anti-apoptotic factor also exhibiting increased levels in bladder cancer. We also clarify that ALKBH8 transgenic mice showed an accelerated rate of bladder tumor mass and invasiveness in an N-butyl-N-(4-hydroxybutyl)-nitrosamine-induced bladder cancer model. These findings suggest that the high expression of ALKBH8 is critical for the growth and progression of bladder cancer.

authors

Ohshio I,Kawakami R,Tsukada Y,Nakajima K,Kitae K,Shimanoe T,Saigo Y,Hase H,Ueda Y,Jingushi K,Tsujikawa K

doi

10.1016/j.bbrc.2016.06.084

subject

Has Abstract

pub_date

2016-08-26 00:00:00

pages

413-8

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(16)31002-6

journal_volume

477

pub_type

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