| we review recent findings that directly impact our understanding of the TGF-beta paradox and discuss their importance to targeting the oncogenic activities of TGF-beta in developing and progressing neoplasms | neoplasm, |
| diminishes T cell surveillance of oncogene-induced prostate cancer | prostate, |
| An increase in endoglin protein expression level may interfere with the oncogenic potential of TGF-beta(1) and TGF-beta type II receptor in endometrial cancer. | endometrial, |
| autocrine TGF-beta signaling is an integral part of the cellular anti-transformation network by suppressing the expression of a host of genes, including p21-regulated genes, that mediate oncogene-induced transformation in basal-like breast cancer. | breast, |
| HOXB9 overexpression increased the tumorigenicity of glioma cells in vivo. Moreover, the activation of transforming growth factor-beta1 contributed to HOXB9-induced oncogenic activities. | glioma, |
| Findings identify Ucn as a potential mediator that inhibits TGFbeta1 oncogenic signaling in breast neoplasm. | neoplasm,breast, |
| fibroblast transcriptional programming in response to TGF-beta1 during development, oncogenesis, tissue repair, and fibrosis | None |
| TGF-ss signaling in fibroblasts differentially affects epithelial growth and oncogenesis | None |
| specific signaling functions and induction of genes differentially required for enhanced effect of EGF- and TGF-beta1-induced oncogenic properties | None |
| finite lifespan human mammary epithelial cells undergo a p16/RB- and p53-independent Oncogene-induced senescence in response to oncogenic RAS that requires TGF-beta signaling | None |
| Thus, oncogenic Ras and TGF-beta signaling stimulate cancer progression through activation of the DeltaNp63 transcriptional program. | None |
| these results define the oncogenic effects of the GARP-TGFbeta axis in the tumor microenvironment | None |
| analysis of how the molecular mechanisms involved in the dual response to TGF-beta in cancer, and how tumor cells evolve to evade the tumor-suppressive responses of this signaling pathway and then hijack the signal, converting it into an oncogenic factor [review] | None |
| These findings identify SOX4 as an important SMAD3 co-factor controlling transcription of pro-metastatic genes and context-dependent shaping of the cellular response to TGF-b. Targeted disruption of the interaction between these factors may have the potential to disrupt pro-oncogenic TGF-b signaling, thereby impairing tumorigenesis. | None |
| TGFBI silencing significantly inhibits PDAC tumor development in a chick chorioallantoic membrane assay model. Our study highlights TGFBI as an oncogenic extracellular matrix interacting protein that bears the potential to serve as a target for new anti-PDAC therapeutic strategies | None |