Ornithine decarboxylase over‐expression stimulates mitogen‐activated protein kinase and anchorage‐independent growth of human breast epithelial cells

Ornithine decarboxylase overexpression enhances ERK and p38 phosphorylation and matrix metalloproteinase‐2 expression

“…In the present study, we found that ODC overexpression induced phosphorylated Erk. The data are consistent with previous reports (Kubota et al, 1997;Manni et al, 1997). In addition to Erk activation, we found that ODC overexpression induced p38 MAP kinase activation.…”

Depletion of Polyamines and Increase of Transforming Growth Factor‐β1, c‐myc, Collagen‐Type I, Matrix Metalloproteinase‐1, and Metalloproteinase‐2 mRNA in Primary Human Gingival Fibroblasts

“…C-myc and TGF-β 1 mRNA levels were related (P ≤0.01) to MMP-1, MMP-2, COL-I, and TIMP-1 gene expression after DFMO treatment, while in CT only c-myc showed a significant show they are related to gene expression 3 and it supports other findings suggesting a new role for PA as negative regulators of c-myc expression. 8,28 Moreover, ODC is necessary for triggering mitogen-activated protein kinase cascade, 29 and SPM provokes conformational changes in the kinase; 30 since TGF-β 1 stimulates protein kinase, 31,32 these substances could play a central role in the pathways linking PA to TGF-β 1 , c-myc, MMP-1, MMP-2 and COL-I gene expression. These patterns of mRNA steady-state levels, together with the relationship showing that TGF-β 1 may favor ECM changes, show that the ODC/PA system in human gingival fibroblasts plays an indirect role in the relationship between TGF-β 1 , c-myc, MMP-1, MMP-2, and COL-I gene expression, without interferring in TIMP-1 mRNA synthesis.…”