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|Title:||Endothelin receptor type B counteracts tenascin-C-induced endothelin receptor type A-dependent focal adhesion and actin stress fiber disorganization|
|Source:||Lange, K., Kammerer, M., Hegi, M.E., Grotegut, S., Dittmann, A., Huang, W., Fluri, E., Yip, G.W., Götte, M., Ruiz, C., Orend, G. (2007-07-01). Endothelin receptor type B counteracts tenascin-C-induced endothelin receptor type A-dependent focal adhesion and actin stress fiber disorganization. Cancer Research 67 (13) : 6163-6173. ScholarBank@NUS Repository. https://doi.org/10.1158/0008-5472.CAN-06-3348|
|Abstract:||Tenascin-C, an extracellular matrix molecule of the tumor-specific microenvironment, counteracts the tumor cell proliferation-suppressing effect of fibronectin by blocking the integrin α 5β 1/ syndecan-4 complex. This causes cell rounding and stimulates tumor cell proliferation.T enascin-C also stimulates endothelin receptor type A (EDNRA) expression. Here, we investigated whether signaling through endothelin receptors affects tenascin-C-induced cell rounding. We observed that endothelin receptor type B (EDNRB) activation inhibited cell rounding by tenascin-C and induced spreading by restoring expression and function of focal adhesion kinase (FAK), paxillin, RhoA, and tropomyosin-1 (TM1) via activation of epidermal growth factor receptor, phospholipase C, c-Jun NH 2-terminal kinase, and the phosphatidylinositol 3-kinase pathway.In contrast to EDNRB, signaling through EDNRA induced cell rounding, which correlated with FAK inhibition and TM1 and RhoA protein destabilization in the presence of tenascin-C. This occurred in a mitogen-activated protein kinase/extracellular signal-regulated kinase kinase-dependent manner. Thus, tumorigenesis might be enhanced by tenascin-C involving EDNRA signaling. Inhibition of tenascin-C in combination with blocking both endothelin receptors could present a strategy for sensitization of cancer and endothelial cells toward anoikis. ©2007 American Association for Cancer Research.|
|Source Title:||Cancer Research|
|Appears in Collections:||Staff Publications|
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