| First Author | Cariaga-Martínez AE | Year | 2014 |
| Journal | Biol Open | Volume | 3 |
| Issue | 10 | Pages | 924-36 |
| PubMed ID | 25217619 | Mgi Jnum | J:217307 |
| Mgi Id | MGI:5613738 | Doi | 10.1242/bio.20148185 |
| Citation | Cariaga-Martinez AE, et al. (2014) Phosphoinositide 3-kinase p85beta regulates invadopodium formation. Biol Open 3(10):924-36 |
| abstractText | The acquisition of invasiveness is characteristic of tumor progression. Numerous genetic changes are associated with metastasis, but the mechanism by which a cell becomes invasive remains unclear. Expression of p85beta, a regulatory subunit of phosphoinositide-3-kinase, markedly increases in advanced carcinoma, but its mode of action is unknown. We postulated that p85beta might facilitate cell invasion. We show that p85beta localized at cell adhesions in complex with focal adhesion kinase and enhanced stability and maturation of cell adhesions. In addition, p85beta induced development at cell adhesions of an F-actin core that extended several microns into the cell z-axis resembling the skeleton of invadopodia. p85beta lead to F-actin polymerization at cell adhesions by recruiting active Cdc42/Rac at these structures. In accordance with p85beta function in invadopodium-like formation, p85beta levels increased in metastatic melanoma and p85beta depletion reduced invadopodium formation and invasion. These results show that p85beta enhances invasion by inducing cell adhesion development into invadopodia-like structures explaining the metastatic potential of tumors with increased p85beta levels. |
