The new study shows that one type, MMP-3, causes normal cells to express a protein, Rac1b, that has previously been found only in cancers. Rac1b stimulates the production of highly reactive oxygen molecules, which promote cancer in two ways — by leading to tissue disorganization and by damaging genomic DNA. Changes in the cell skeleton induced by Rac1b trigger the formation of extremely reactive molecules known as reactive oxygen species, or ROS. In turn, the increased amount of ROS activates key genes that control the epithelial-mesenchymal transition — the first slippage in an avalanche of tissue disorganization.
"MMP-3-induced Rac1b stimulates formation of ROS, causing EMT and genomic instability," by Derek C. Radisky, Dinah D. Levy, Laurie E. Littlepage, Hong Liu, Celeste M. Nelson, Jimmie E. Fata, Devin Leake, Elizabeth L. Godden, Donna G. Albertson, M. Angela Nieto, Zena Werb, and Mina J. Bissell, appears in the 7 July 2005 issue of Nature.
Interesante por el hecho de que la modificacion externa, mediada por el estroma, puede incidir en la progresion del cancer. Cubre un vacio en el papel de la estromelisina en el cancer de mama.
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NF-kappaB binds to a polymorphic repressor element in the MMP-3 promoter.Biochem Biophys Res Commun. 2004 Mar 26;316(1):182-8.
These results are consistent with a role for NF-kappaB in limiting the cytokine induced expression of MMP-3.
Por ende NFkB podria reprimir MMP3
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