| First Author | Brentnall M | Year | 2014 |
| Journal | J Cell Sci | Volume | 127 |
| Issue | Pt 10 | Pages | 2217-26 |
| PubMed ID | 24610949 | Mgi Jnum | J:214697 |
| Mgi Id | MGI:5603710 | Doi | 10.1242/jcs.135137 |
| Citation | Brentnall M, et al. (2014) Procaspase-3 regulates fibronectin secretion and influences adhesion, migration and survival independently of catalytic function. J Cell Sci 127(Pt 10):2217-26 |
| abstractText | Caspase-3 is an effector caspase that is activated downstream of mitochondrial outer-membrane permeabilization (MOMP) during apoptosis. However, previous work has demonstrated that caspase-3-deficient mouse embryonic fibroblasts (MEFs) are resistant to mitochondrially mediated cell death and display a delay in the mitochondrial events of apoptosis, including Bax activation, MOMP and release of cytochrome c. Here, we show that caspase-3 regulates fibronectin secretion and impacts on cell morphology, adhesion and migration. Surprisingly, the catalytic activity of caspase-3 is not required for these non-apoptotic functions. Moreover, we found that caspase-3-deficient MEFs are not resistant to death by anoikis and that exogenous fibronectin protects wild-type MEFs from cell death induced by serum withdrawal. Taken together, our data indicate that procaspase-3 has a non-apoptotic function; it regulates the secretion of fibronectin and influences morphology, adhesion and migration. Furthermore, this novel procaspase-3 function might alter the apoptotic threshold of the cell. |
