| First Author | Gervasi M | Year | 2012 |
| Journal | J Cell Biol | Volume | 196 |
| Issue | 5 | Pages | 589-603 |
| PubMed ID | 22391036 | Mgi Jnum | J:185061 |
| Mgi Id | MGI:5427296 | Doi | 10.1083/jcb.201109045 |
| Citation | Gervasi M, et al. (2012) JunB contributes to Id2 repression and the epithelial-mesenchymal transition in response to transforming growth factor-beta. J Cell Biol 196(5):589-603 |
| abstractText | The process of epithelial-mesenchymal transition (EMT) in response to transforming growth factor-beta (TGF-beta) contributes to tissue fibrosis, wound healing, and cancer via a mechanism that is not fully understood. This study identifies a critical role of JunB in the EMT and profibrotic responses to TGF-beta. Depletion of JunB by small interfering ribonucleic acid abrogates TGF-beta-induced disruption of cell-cell junctions, formation of actin fibers, focal adhesions, and expression of fibrotic proteins. JunB contributes to Smad-mediated repression of inhibitor of differentiation 2 through interaction with transcription repressor activating transcription factor 3. Importantly, JunB mediates the TGF-beta induction of profibrotic response factors, fibronectin, fibulin-2, tropomyosin (Tpm1), and integrin-beta3, which play critical roles in matrix deposition, cell-matrix adhesion, and actin stress fibers. In summary, JunB provides important input in setting the transcriptional program of the EMT and profibrotic responses to TGF-beta. Thus, JunB represents an important target in diseases associated with EMT, including cancer and fibrosis. |
