Correlation between T lymphoma invasion and metastasis 1 expression and epithelial-mesenchymal transition in human colorectal carcinomas / 南方医科大学学报
Journal of Southern Medical University
;
(12): 232-235, 2009.
Artigo
em Chinês
| WPRIM
| ID: wpr-339023
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the relationship between T lymphoma invasion and metastasis 1 (Tiam1) and epithelial-mesenchymal transition (EMT) in human colorectal carcinomas.</p><p><b>METHODS</b>Tiam1, E-cadherin, CK, and vimentin expressions in normal colorectal epithelium, colorectal carcinomas (CRC) and CRC with lymphatic metastasis were determined by immunohistochemistry using a two-step method.</p><p><b>RESULTS</b>Tiam1 expression was significantly higher in CRC than in normal colorectal epithelium (P<0.01) in close correlation to the degree of tumor differentiation (P<0.05). Higher Tiam1 expression was detected in CRC with lymphatic metastasis than in primary CRC (P<0.05). The expressions of E-cadherin and CK in CRC tissues were significantly lowered in comparison with those in normal colorectal epithelium (P<0.01), showing a correlation to tumor differentiation (P<0.01) but not to lymphatic metastasis. Vimentin was significantly overexpressed in CRC (P<0.01) and correlated to tumor differentiation (P<0.01) but not to lymphatic metastasis. Tiam1 expression was inversely correlated to E-cadherin and CK, but positively to vimentin.</p><p><b>CONCLUSION</b>Tiam1 is related to the metastasis of colorectal carcinoma, and may induce EMT to promote CRC metastasis.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Patologia
/
Fisiologia
/
Neoplasias Colorretais
/
Adenocarcinoma
/
Caderinas
/
Movimento Celular
/
Fatores de Troca do Nucleotídeo Guanina
/
Células Epiteliais
/
Transdiferenciação Celular
/
Proteína 1 Indutora de Invasão e Metástase de Linfoma de Células T
Limite:
Adulto
/
Idoso
/
Aged80
/
Feminino
/
Humanos
/
Masculino
Idioma:
Chinês
Revista:
Journal of Southern Medical University
Ano de publicação:
2009
Tipo de documento:
Artigo
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