| First Author | Angel I | Year | 2020 |
| Journal | Oncogene | Volume | 39 |
| Issue | 46 | Pages | 6990-7004 |
| PubMed ID | 33077835 | Mgi Jnum | J:299442 |
| Mgi Id | MGI:6477648 | Doi | 10.1038/s41388-020-01506-6 |
| Citation | Angel I, et al. (2020) Tenascin C promotes cancer cell plasticity in mesenchymal glioblastoma. Oncogene 39(46):6990-7004 |
| abstractText | Interconversion of transformed non-stem cells to cancer stem cells, termed cancer cell plasticity, contributes to intra-tumor heterogeneity and its molecular mechanisms are currently unknown. Here, we have identified Tenascin C (TNC) to be upregulated and secreted in mesenchymal glioblastoma (MES GBM) subtype with high NF-kappaB signaling activity. Silencing TNC decreases proliferation, migration and suppresses self-renewal of glioma stem cells. Loss of TNC in MES GBM compromises de-differentiation of transformed astrocytes and blocks the ability of glioma stem cells to differentiate into tumor derived endothelial cells (TDEC). Inhibition of NF-kappaB activity or TNC knockdown in tumor cells decreased their tumorigenic potential in vivo. Our results uncover a link between NF-kappaB activation in MES GBM and high levels of TNC in GBM extracellular matrix. We suggest that TNC plays an important role in the autocrine regulation of glioma cell plasticity and hence can be a potential molecular target for MES GBM. |
