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Open Access Research article

ABI3 ectopic expression reduces in vitro and in vivo cell growth properties while inducing senescence

Flavia RM Latini1, Jefferson P Hemerly1, Beatriz CG Freitas1, Gisele Oler1, Gregory J Riggins2 and Janete M Cerutti1*

Author Affiliations

1 Genetic Bases of Thyroid Tumors Laboratory, Division of Genetics and Division of Endocrinology, Universidade Federal de São Paulo, SP, Brazil

2 Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA

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BMC Cancer 2011, 11:11  doi:10.1186/1471-2407-11-11

Published: 11 January 2011

Abstract

Background

Mounting evidence has indicated that ABI3 (

    ABI
family member
    3
) function as a tumor suppressor gene, although the molecular mechanism by which ABI3 acts remains largely unknown.

Methods

The present study investigated ABI3 expression in a large panel of benign and malignant thyroid tumors and explored a correlation between the expression of ABI3 and its potential partner ABI3-binding protein (ABI3BP). We next explored the biological effects of ABI3 ectopic expression in thyroid and colon carcinoma cell lines, in which its expression was reduced or absent.

Results

We not only observed that ABI3 expression is reduced or lost in most carcinomas but also that there is a positive correlation between ABI3 and ABI3BP expression. Ectopic expression of ABI3 was sufficient to lead to a lower transforming activity, reduced tumor in vitro growth properties, suppressed in vitro anchorage-independent growth and in vivo tumor formation while, cellular senescence increased. These responses were accompanied by the up-regulation of the cell cycle inhibitor p21 WAF1 and reduced ERK phosphorylation and E2F1 expression.

Conclusions

Our result links ABI3 to the pathogenesis and progression of some cancers and suggests that ABI3 or its pathway might have interest as therapeutic target. These results also suggest that the pathways through which ABI3 works should be further characterized.