Latency of cathepsin B secreted by human colon carcinoma cells is not linked to secretion of cystacin C and is relieved by neutrophil elastase
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, ISSN: 0925-4439, Vol: 1226, Issue: 2, Page: 117-125
1994
- 46Citations
- 10Captures
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Metrics Details
- Citations46
- Citation Indexes46
- 46
- CrossRef35
- Captures10
- Readers10
- 10
Article Description
The lysosomal cystein proteinase cathepsin B is shown to be secreted by ten human colon carcinoma cell lines and to accumulate in culture media as a latent enzyme. The cell lines also secrete a physiological inhibitor of cathepsin B, cystatin C. A significant correlation was found between secretion of the latent enzyme and the inhibitor ( r = 0.755, P < 0.01). The aim of the present study was to modulate the respective secretion of the two antagonists to test whether or not latency of cathepsin B was due to the concomitant secretion of the inhibitor. SW480 colon carcinoma cells were treated with the acidotropic agent ammonium chloride, phorbol 12-myristate 13-acetate, and the inflammatory cytokines TGF-β, TNF-α, and IL-1β. Ammonium chloride significantly increased latent cathepsin B levels without affecting the constitutive secretion of cystatin C. Phorbol 12-myristate 13-acetate induced a 4- to 5-fold increase in secreted latent cathepsin B, but did not alter significantly the accumulation of cystatin C in media. The cytokines, TGF-β, TNF-α, and IL-1β, had no major effect on the expression of these two antagonists. Latent cathepsin B released from human carcinoma cells could be efficiently activated by neutrophil elastate at neutral pH. It is concluded that latent cathepsin B is a true proenzyme rather than an enzyme-inhibitor comples. In addition, our data from neutrophil elastate activation experiments indicate that a proteolytic system for activation of the tumor cell-secreted latent enzyme may exist in vivo.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/0925443994900183; http://dx.doi.org/10.1016/0925-4439(94)90018-3; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0028356053&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/8204657; https://linkinghub.elsevier.com/retrieve/pii/0925443994900183; http://dx.doi.org/10.1016/0925-4439%2894%2990018-3
Elsevier BV
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