ISSN:
1573-7276
Keywords:
activation
;
cAMP
;
Concanavalin A
;
gelatinase A
;
human breast cancer
;
MT-MMP
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract We have previously reported that induction of MMP-2 activation by Concanavalin A (ConA) in MDA-MB-231human breast cancer cells involves both transcriptional and post-transcriptional mechanisms, and that the continuous presence of ConA is required for MMP-2 activation (Yu et al. Cancer Res, 55, 3272-7, 1995).In an effort to identify signal transduction pathways which may either contribute to or modulate this mechanism,we found that three different cAMP-inducing agents, cholera toxin (CT), forskolin (FSK), and3-isobutyl-1-methylxanthine (IBMX) partially inhibited ConA-induced MT1-MMP expression and MMP-2activation in MDA-MB-231 cells. Combinations of CT or FSK with IBMX exhibited additive effects on reduction of MT1-MMP mRNA expression and MMP-2 activation. Agents which increase cAMP levels appeared to target transcriptional aspects of ConA induction, reducing MT1-MMP mRNA and protein in parallel with the reduced MMP-2 activation. In the absence of ConA, down-regulation of constitutive production of MT1-MMP mRNA and protein was observed, indicating that cAMP acts independently of ConA. These observations may help to elucidate factors regulating MT1-MMP expression, which may be pivotal to the elaboration of invasive machinery on the cell surface. © Rapid Science 1998
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1023/A:1006580406314
