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Titolo:
Regulation of cellular invasion and matrix metalloproteinase activity in HepG2 cell by connexin 26 transfection
Autore:
Yano, T; Yamasaki, H;
Indirizzi:
Kwansei Gakuin Univ, Fac Sci, Nishinomiya, Hyogo 662, Japan Kwansei GakuinUniv Nishinomiya Hyogo Japan 662 inomiya, Hyogo 662, Japan Int Agcy Res Canc, Unit Multistage Carcinogenesis, F-69372 Lyon, France Int Agcy Res Canc Lyon France F-69372 rcinogenesis, F-69372 Lyon, France
Titolo Testata:
MOLECULAR CARCINOGENESIS
fascicolo: 2, volume: 31, anno: 2001,
pagine: 101 - 109
SICI:
0899-1987(200106)31:2<101:ROCIAM>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
E-CADHERIN; HEPATOCELLULAR-CARCINOMA; INTERCELLULAR COMMUNICATION; GAP-JUNCTIONS; EXPRESSION; TUMOR; RAT; METASTASIS; CATENINS; ADHESION;
Keywords:
beta-catenin; E-cadherin; gap junction intercellular communication; human hepatocellular carcinoma; negative growth control;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Yamasaki, H Kwansei Gakuin Univ, Fac Sci, 1-1-115 Uegahara, Nishinomiya, Hyogo 662, Japan Kwansei Gakuin Univ 1-1-115 Uegahara Nishinomiya Hyogo Japan 662
Citazione:
T. Yano e H. Yamasaki, "Regulation of cellular invasion and matrix metalloproteinase activity in HepG2 cell by connexin 26 transfection", MOL CARCINO, 31(2), 2001, pp. 101-109

Abstract

We previously reported that connexin (Cx) 26 expression is involved in negative growth control of HepG2 cells established from a human hepatoma. We also found that induction of E-cadherin and subsequent formation of a cell adhesion complex were induced in HepG2 cells by Cx26 expression. To examine the exact role of Cx26-induced E-cadherin junctions in regulating appearance of malignant phenotypes of HepG2 cells, we expressed a Cx26 antisense oligodeoxynucleotide (AS-ODN) in an established HepG2 cell clone that has stable expression of Cx26 genes. We investigated changes in the expression of E-cadherin, the localization of beta -catenin, and some malignant phenotypesof HepG2 clone after the suppression of Cx26 expression by AS-ODN treatment. The AS-ODN treatment prevented the expression of Cx26 and E-cadherin, and the localization of beta -catenin was changed from cytoplasmic membrane to the cytoplasm. In parallel, a morphological change from a monolayer of polygonal cells to multilayered colonies was induced by the treatment, indicating a change of a malignant phenotype of HepG2 cells. The activity of matrix metalloproteinase 9 (MMP-9) was elevated by the AS-ODN treatment. A concomitant increase in invasiveness of the Cx26-expressing cells by the treatment was also observed in an in vitro assay with Matrigel matrix. These results suggest that the induction of E-cadherin and formation of the cell adhesion complex by Cx26 expression contribute to the reversal of some malignant phenotypes of HepG2 cells. Furthermore, the Cx26-dependent expression of E-cadherin leads to reduction of the invasiveness of the cells through suppression of MMP-9 activity. (C) 2001 Wiiey-Liss. Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/05/20 alle ore 13:29:52