Re-expression of ABI3-binding protein suppresses thyroid tumor growth by promoting senescence and inhibiting invasion

Re-expression of ABI3-binding protein suppresses thyroid tumor growth by promoting senescence and inhibiting invasion

Autor Latini, Flavia Roche Moreira Autor UNIFESP Google Scholar
Hemerly, Jefferson Pessoa Autor UNIFESP Google Scholar
Oler, Gisele Autor UNIFESP Google Scholar
Riggins, Gregory J. Google Scholar
Cerutti, Janete Maria Autor UNIFESP Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Johns Hopkins Univ
Resumo Loss of ABI gene family member 3-binding protein (ABI3BP) expression may be functionally involved in the pathogenesis of cancer. Previous reports have indicated a loss of expression in lung cancer and a presumed role in inducing cellular senescence. We show here that ABI3BP expression is significantly decreased in most malignant thyroid tumors of all types. To better understand ABI3BPs role, we created a model by re-expressing ABI3BP in two thyroid cancer cell lines. Re-expression of ABI3BP in thyroid cells resulted in a decrease in transforming activity, cell growth, cell viability, migration, invasion, and tumor growth in nude mice. ABI3BP re-expression appears to trigger cellular senescence through the p21 pathway. Additionally, ABI3BP induced formation of heterochromatin 1-binding protein gamma-positive senescence-associated (SA) heterochromatin foci and accumulation of SA beta-galactosidase. the combination of a decrease in cell growth, invasion, and other effects upon ABI3BP re-expression in vitro helps to explain the large reduction in tumor growth that we observed in nude mice. Together, our data provide evidence that the loss of ABI3BP expression could play a functional role in thyroid tumorigenesis. Activation of ABI3BP or its pathway may represent a possible basis for targeted therapy of certain cancers. Endocrine-Related Cancer (2008) 15 787-799
Idioma Inglês
Financiador NIH
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Número do financiamento NIH: CA113461
FAPESP: 04/15288-0
FAPESP: 05/60330-8
Data 2008-09-01
Publicado em Endocrine-related Cancer. Bristol: Soc Endocrinology, v. 15, n. 3, p. 787-799, 2008.
ISSN 1351-0088 (Sherpa/Romeo, fator de impacto)
Editor Soc Endocrinology
Extensão 787-799
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000259965200011

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