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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.

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