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Oxidative stress specifically downregulates survivin to promote breast tumour formation.

Abstract：

BACKGROUND:Breast cancer, a heterogeneous disease has been broadly classified into oestrogen receptor positive (ER+) or oestrogen receptor negative (ER-) tumour types. Each of these tumours is dependent on specific signalling pathways for their progression. While high levels of survivin, an anti-apoptotic protein, increases aggressive behaviour in ER- breast tumours, oxidative stress (OS) promotes the progression of ER+ breast tumours. Mechanisms and molecular targets by which OS promotes tumourigenesis remain poorly understood. RESULTS:DETA-NONOate, a nitric oxide (NO)-donor induces OS in breast cancer cell lines by early re-localisation and downregulation of cellular survivin. Using in vivo models of HMLE(HRAS) xenografts and E2-induced breast tumours in ACI rats, we demonstrate that high OS downregulates survivin during initiation of tumourigenesis. Overexpression of survivin in HMLE(HRAS) cells led to a significant delay in tumour initiation and tumour volume in nude mice. This inverse relationship between survivin and OS was also observed in ER+ human breast tumours. We also demonstrate an upregulation of NADPH oxidase-1 (NOX1) and its activating protein p67, which are novel markers of OS in E2-induced tumours in ACI rats and as well as in ER+ human breast tumours. CONCLUSION:Our data, therefore, suggest that downregulation of survivin could be an important early event by which OS initiates breast tumour formation.

journal_name

Br J Cancer

journal_title

British journal of cancer

authors

Pervin S,Tran L,Urman R,Braga M,Parveen M,Li SA,Chaudhuri G,Singh R

doi

10.1038/bjc.2013.40

subject

Has Abstract

pub_date

2013-03-05 00:00:00

pages

848-58

issue

4

eissn

0007-0920

issn

1532-1827

pii

bjc201340

journal_volume

108

pub_type

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