Downregulated inhibitor of growth 3 (ING3) expression during colorectal carcinogenesis.
Indian J Med Res
; 139(4): 561-7, 2014 Apr.
Article
em En
| MEDLINE
| ID: mdl-24927342
ABSTRACT
BACKGROUND & OBJECTIVES:
ING3 (inhibitor of growth protein 3) overexpression decreased S-phase cell population and colony-forming efficiency, and induced apoptosis at a p53-mediated manner. The aim of this study was to investigate the clinicopathological and prognostic significance of ING3 expression in colorectal carcinogenesis and subsequent progression.METHODS:
ING3 expression was examined by immunohistochemistry on tissue microarray containing colorectal non-neoplastic mucosa (NNM), adenoma and adenocarcinoma. Colorectal carcinoma tissue and cell lines were studied for ING3 expression by Western blot or RT-PCR.RESULTS:
ING3 mRNA was differentially expressed in Colo201, Colo205, DLD-1, HCT-15, HCT-116, HT-29, KM-12, SW480, SW620 and WiDr cells. Carcinomas showed significantly lower ING3 expression than matched NNM at mRNA level (P< 0.05), but not at protein level. Immunohistochemically, ING3 expression was significantly decreased from NNM, adenoma to adenocarcinoma (P< 0.05). ING3 expression was not correlated with age, sex, tumour size, depth of invasion, lymphatic or venous invasion, lymph node metastasis, tumour- node- metastasis staging or differentiation. Kaplan-Meier analysis indicated that ING3 protein expression was not associated the prognosis of the patients with colorectal carcinoma (P< 0.05). INTERPRETATION &CONCLUSIONS:
Our study showed that downregulated ING3 expression might play an important role in colorectal adenoma-adenocarcinoma sequence. Further studies are required to understand the mechanism.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias Colorretais
/
Regulação Neoplásica da Expressão Gênica
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Proteínas de Homeodomínio
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Proteínas Supressoras de Tumor
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Carcinogênese
Limite:
Humans
País/Região como assunto:
Asia
Idioma:
En
Revista:
Indian J Med Res
Ano de publicação:
2014
Tipo de documento:
Article