cathepsin b mediates the ph-dependent proinvasive activity of tumor-shed microvesicles
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ID: 174288
2008
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Abstract
Vesicles shed by cancer cells are known to mediate several tumor-host interactions. Tumor microenvironment may, in turn, influence the release and the activity of tumor-shed microvesicles. In this study, we investigated the molecular mediators of the pH-dependent proinvasive activity of tumor-shed vesicles. Gelatinase zymography showed increased microvesicle activity of matrix metalloproteinases 9 and 2 as a result of acid exposure (pH 5.6) compared to pH 7.4. Thus, we reasoned that the cysteine protease cathepsin B might play a role in mediating the pH-dependent activation of gelatinases. Cathepsin B expression in tumor-shed microvesicles was confirmed by Western blot analysis and zymography. The activity of vesicle-associated cathepsin B measured using Z-Arg-Arg-pNA as substrate was significantly increased at acidic pH values. Inhibition of protease activity by the cysteine protease inhibitor, E-64, and treatment of ovarian cancer cells with small interfering RNA against cathepsin B suppressed the ability of tumor-shed microvesicles to stimulate both gelatinase activation and the invasiveness of endothelial cells observed at low pH values. We conclude that microvesicle shedding is a major secretory pathway for cathepsin B release from tumor cells. Hence, the acidic microenvironment found in most solid tumors may contribute to cathepsin B-mediated proinvasive capabilities of tumor-shed vesicles.
| Reference Key |
giusti2008neoplasia:cathepsin
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|---|---|
| Authors | ;Ilaria Giusti;Sandra D’Ascenzo;Danilo Millimaggi;Giulia Taraboletti;Gaspare Carta;Nicola Franceschini;Antonio Pavan;Vincenza Dolo |
| Journal | ACS chemical neuroscience |
| Year | 2008 |
| DOI |
10.1593/neo.08178
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| URL | |
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