Effect of Ca2+ mobilization on release and activation of matrix metalloproteinases in hepatocellular carcinoma cells / 中华肿瘤杂志
Chinese Journal of Oncology
; (12): 525-527, 2004.
Article
em Zh
| WPRIM
| ID: wpr-254310
Biblioteca responsável:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of Ca(2+) mobilization on release and activation of matrix metalloproteinases (MMPs) in human hepatocellular carcinoma cells.</p><p><b>METHODS</b>Ca(2+) and chemicals which can induce or inhibit Ca(2+) mobilization were added into human SMMC-7721 hepatoma cells in vitro. SDS-PAGE protein electrophoresis and gelatin zymography analysis were carried out to detect the changes of release and activation of MMPs in the cell culture supernatant.</p><p><b>RESULTS</b>Addition of CaCl(2) into culture system resulted in an enhanced secretion and activation of MMP-2 and MMP-9 in a dose-dependent manner. At a dose of 0.8 mmol/L CaCl(2), it maintained a stable high level of MMPs, especially of MMP-2 with (109.71 +/- 27.93)% elevation as compared to the cells without CaCl(2) addition (P < 0.001). SDS-PAGE analysis showed that most secreted proteins were MMPs (MMP-2 and MMP-9) when the cells cultured in media without serum. Thapsigargin (Tg, 4 micromol/L), an inducer of intracellular Ca(2+) stores depletion, significantly enhanced the release and activation of MMP-2 and MMP-9, compared to the control with (58.63 +/- 31.04)% elevation (P < 0.05), while the inducing effect of Tg on MMPs release and activation was significantly inhibited by S-nitro-N-acetylpenicillamine (SNAP, 200 micromol/L), an NO donor.</p><p><b>CONCLUSION</b>Intracellular Ca(2+) regulation pathways may play an important role in the process of release and activation of MMPs.</p>
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Índice:
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Assunto principal:
Patologia
/
Penicilamina
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Farmacologia
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Cálcio
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Carcinoma Hepatocelular
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Tapsigargina
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Secreções Corporais
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Doadores de Óxido Nítrico
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Metaloproteinase 2 da Matriz
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Metaloproteinase 9 da Matriz
Limite:
Humans
Idioma:
Zh
Revista:
Chinese Journal of Oncology
Ano de publicação:
2004
Tipo de documento:
Article