1,721,079 research outputs found
The interaction of leucocytes with vascular endothelial cells in vitro with respect to experimental inflammation in the rat
No full textOpposing roles for specific TIMPs in breast cancer prognostic
No full textThe two articles (Span et al. 2004 and Schrohl et al.
2004) highlight the complexity and specificity of
matrix metalloproteinases (MMPs) and TIMPs in
cancer biology, diagnosis, and treatment. Both provide
novel insights into these issues by focussing on
TIMPs rather than MMPs and extend a growing
number of reports that the roles played by TIMPs in
tumour pathology may be much broader than the
inhibition of MMP action on the extracellular matrix
(ECM), and may extend to the regulation of MMP
influence on many systems and potentially to MMPindependent
functions. Specific TIMP-3 involvement
in tamoxifen-induced apoptosis strongly contrasts
the association between elevated TIMP-1 levels with
poor outcome in breast cancer. Although candidate
apoptotic mechanisms may elegantly explain the effect
of TIMP-3 results, the reasons underlying the TIMP-1
result remain to be fully elucidated
Gelatinase B/MMP-9 in Tumour Pathogenesis and Progression
Get PDFSince its original identification as a leukocyte gelatinase/type V collagenase and tumour type IV collagenase, gelatinase B/matrix metalloproteinase (MMP)-9 is now recognised as playing a central role in many aspects of tumour progression. In this review, we relate current concepts concerning the many ways in which gelatinase B/MMP-9 influences tumour biology. Following a brief outline of the gelatinase B/MMP-9 gene and protein, we analyse the role(s) of gelatinase B/MMP-9 in different phases of the tumorigenic process, and compare the importance of gelatinase B/MMP-9 source in the carcinogenic process. What becomes apparent is the importance of inflammatory cell-derived gelatinase B/MMP-9 in tumour promotion, early progression and triggering of the “angiogenic switch”, the integral relationship between inflammatory, stromal and tumour components with respect to gelatinase B/MMP-9 production and activation, and the fundamental role for gelatinase B/MMP-9 in the formation and maintenance of tumour stem cell and metastatic niches. It is also apparent that gelatinase B/MMP-9 plays important tumour suppressing functions, producing endogenous angiogenesis inhibitors, promoting inflammatory anti-tumour activity, and inducing apoptosis. The fundamental roles of gelatinase B/MMP-9 in cancer biology underpins the need for specific therapeutic inhibitors of gelatinase B/MMP-9 function, the use of which must take into account and substitute for tumour-suppressing gelatinase B/MMP-9 activity and also limit inhibition of physiological gelatinase B/MMP-9 function
STUDIES ON THE EFFECTS OF LAMININ, E-8 FRAGMENT OF LAMININ AND SYNTHETIC LAMININ PEPTIDES PA22-2 AND YIGSR ON MATRIX METALLOPROTEINASES AND TISSUE INHIBITOR OF METALLOPROTEINASE EXPRESSION
No full textEXPRESSION OF 72 KD GELATINASE AND TYPE-IV COLLAGEN DURING CARBON TETRACHLORIDE-INDUCED RAT-LIVER FIBROSIS
No full text
The alternative TrkAIII splice variant expressed by human neuroblastomas and glioblastomas targets the centrosome and promotes genetic instability
No full textBASEMENT-MEMBRANE TYPE-IV COLLAGEN DEGRADATION - EVIDENCE FOR THE INVOLVEMENT OF A PROTEOLYTIC CASCADE INDEPENDENT OF METALLOPROTEINASES
No full textCurrent hypotheses suggest that both the plasmin system and metalloproteinases
are involved in tumor invasion of basement membrane. In
this study, we demonstrate that plasmin can directly degrade native and
denatured type IV collagen in solution as well as in tissue sections. Tumor
cell lines secreted plasminogen activators into culture supernatants that
activated exogenous plasminogen to degrade type IV collagen in zymograms
and to remove collagen IV immunoreactivity from tissue sections.
Inhibition of metalloproteinase activity in culture supernatants by EDTA
did not interfere with plasminogen-mediated type IV collagen degrada
tion. We propose that tumor cells possess a mechanism for the degra
dation of basement membrane type IV collagen, independent of metalloproteinases
but dependent on plasminogen conversion to plasmin
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