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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
Authors: Lange, K.
Kammerer, M.
Hegi, M.E.
Grotegut, S.
Dittmann, A.
Huang, W.
Fluri, E.
Yip, G.W. 
Götte, M.
Ruiz, C.
Orend, G.
Issue Date: 1-Jul-2007
Citation: 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.
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
ISSN: 00085472
DOI: 10.1158/0008-5472.CAN-06-3348
Appears in Collections:Staff Publications

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