Expression of mRNA for membrane-type 1, 2, and 3 matrix metalloproteinases in human laryngeal cancer / 中国医学科学杂志(英文版)
Chinese Medical Sciences Journal
;
(4): 170-173, 2004.
Artigo
em Inglês
| WPRIM
| ID: wpr-253997
ABSTRACT
<p><b>OBJECTIVE</b>To investigate correlation of expressions of membrane-type 1, 2, and 3 matrix metalloproteinases (MT1, MT2, and MT3-MMP) to the invasion and metastases in laryngeal cancer.</p><p><b>METHODS</b>Reverse transcription-polymerase chain reaction (RT-PCR) was used to examine the mRNA level of MT1, MT2, and MT3-MMP in 24 patients with laryngeal cancer. The relationships of these three MT-MMP expressions to clinicopathology were analyzed by statistics.</p><p><b>RESULTS</b>The expressions of MT1, MT2, and MT3-MMP were significantly higher in laryngeal cancer tissues than those in para-tumorous tissues (P < 0.01) and had a close relationship with invasive depth (P < 0.05). But no significantly different expressions of these three MT-MMPs were found in different primary location and different histological grade of laryngeal cancer (P > 0.05). The expression of MT1-MMP was obviously higher in patients with metastatic lymph nodes than that in patients without metastatic lymph nodes (P < 0.05).</p><p><b>CONCLUSION</b>MT1, MT2, and MT3-MMP play an important role in the progression of laryngeal cancer, and MT1-MMP may serve as a reliable marker in estimating invasive and metastatic potency of laryngeal cancer. Suppressing expressions of MT1, MT2, and MT3-MMP early may inhibit the invasion and metastases of laryngeal cancer.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Patologia
/
RNA Mensageiro
/
Metaloendopeptidases
/
Biomarcadores Tumorais
/
Regulação Neoplásica da Expressão Gênica
/
Neoplasias Laríngeas
/
Metaloproteinases da Matriz Associadas à Membrana
/
Metaloproteinase 16 da Matriz
/
Genética
/
Laringe
Limite:
Adulto
/
Idoso
/
Feminino
/
Humanos
/
Masculino
Idioma:
Inglês
Revista:
Chinese Medical Sciences Journal
Ano de publicação:
2004
Tipo de documento:
Artigo
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