Tenascin-C Is a Novel RBPJκ-Induced Target Gene for Notch Signaling in Gliomas

Abstract

Tenascin-C

Tenascins and the Importance of Adhesion Modulation

“…Tenascin-C is strongly implicated in mediating the invasive behavior of glioma cells, and early studies showed that tenascin-C stimulated fibronectinmediated cell migration (Deryugina and Bourdon 1996). Similar observations have been made by several different research groups (Hirata et al 2009;Sivasankaran et al 2009); in one report, this migration was found to be dependent on the induction of metalloproteinase-12 (Sarkar et al 2006). The connection between tenascin-C expression and invasion is, however, not restricted to brain tumors.…”

“…Examples of breast and colon carcinomas are shown in Figure 4. In other cancers such as melanoma or glioblastoma, the cancer cells themselves are secreting tenascin-C (Natali et al 1990;Herlyn et al 1991;Sivasankaran et al 2009) and both tenascin-C as well as tenascin-W are present in brain cancer blood vessels (Higuchi et al 1993;Zagzag et al 1995;Kim et al 2000;Martina et al 2009). Tenascin-W staining correlates with von Willebrand factor staining, which is consistent with tenascin-W production by endothelial cells (Fig.…”

Oct-4+/Tenascin C+ neuroblastoma cells serve as progenitors of tumor-derived endothelial cells

“…Thus, TNC + /Oct-4 + cells grew as neurospheres in vitro for many passages, a feature typical of tumor stem/progenitor cells [35,68]. These neurospheres expressed stem cell-related markers such as βIII-tubulin, HIF-2α, nestin and Notch-2, which controls TNC expression and angiogenesis [69]. Three lines of evidence demonstrated unambiguously that TNC + /Oct-4 + cells were the progenitors of NBderived ECs, and namely (i) in vitro these cells, but not their TNC − counterparts, differentiated into endotheliallike cells expressing VE-cadherin, PSMA and to a lesser extent CD31 after culture with VEGF, and (ii) in vivo TNC + , but not TNC − HTLA-230 cells, formed ortothopic tumors in which a half of the EMs were lined by NB-derived ECs.…”

N-Aryl-N′-(chroman-4-yl)ureas and thioureas display in vitro anticancer activity and selectivity on apoptosis-resistant glioblastoma cells: Screening, synthesis of simplified derivatives, and structure–activity relationship analysis

“…Therefore, it was decided to examine the in vitro effects of these chroman-type potassium-channel openers and related structures on the growth of three human highgrade glioma cell lines, i.e. U373 and T98G from astroglial origin [25e27] and Hs683 from oligodendroglial origin [25,26,28]. While the Hs683 model displays actual sensitivity to pro-apoptotic stimuli [25,29], the U373 [25,29] and T98G [29] models do not.…”