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Enhanced expression of Hab18g/CD147 and activation of integrin pathway in HCC cells under 3-D co-culture conditions.
Wu, Ya-Mei; Tang, Juan; Zhao, Pu; Chen, Zhi-Nan; Jiang, Jian-Li.
Afiliação
  • Wu YM; Cell Engineering Research Centre & Department of Cell Biology, State Key Laboratory of Cancer Biology, The Fourth Military Medical University, 17 West Changle Road, Xi'an 710032, People's Republic of China.
Cell Biol Int ; 33(2): 199-206, 2009 Feb.
Article em En | MEDLINE | ID: mdl-19059491
ABSTRACT
CD147 is reported to be correlated with the malignancy of some cancers, and its overexpression affects the progression of tumor. In the present study, we investigated the function of HAb18G/CD147, a member of CD147 family, on hepatocellular carcinoma (HCC) adhesion, invasion and metastasis in 3-dimensional (3-D) cell co-culture model. The results showed that the extracellular microenvironment could determine the cellular phenotypes and then affected the cellular functions. The expressions of HAb18G/CD147 in HCC cells and fibroblasts were both obviously elevated in 3-D co-culture model. The overexpression of HAb18G/CD147 increased MMPs' (MMP-2 and MMP-9) production (P < 0.01), and was obviously accompanied with enhanced expressions of paxillin, FAK and p-FAK in 3-D cell co-culture model. All the results suggest that HAb18G/CD147 plays an important role in HCC adhesion, invasion and metastasis mainly via modulating synthesis of MMPs and activating integrin signal pathways in fibroblasts and tumor cells themselves under the 3-D co-culture conditions.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Integrinas / Carcinoma Hepatocelular / Basigina / Neoplasias Hepáticas Limite: Adult / Humans / Male Idioma: En Ano de publicação: 2009 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Integrinas / Carcinoma Hepatocelular / Basigina / Neoplasias Hepáticas Limite: Adult / Humans / Male Idioma: En Ano de publicação: 2009 Tipo de documento: Article