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Role of CXCR4/SDF-1 alpha in the migratory phenotype of hepatoma cells that have undergone epithelial-mesenchymal transition in response to the transforming growth factor-beta.
(IDIBELL), Barcelona, Spain.
(IDIBELL), Barcelona, Spain.
(IDIBELL), Barcelona, Spain.
(IDIBELL), Barcelona, Spain.
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2009 (English)In: Cellular Signalling, ISSN 0898-6568, E-ISSN 1873-3913, Vol. 21, no 11, p. 1595-1606Article in journal (Refereed) Published
Abstract [en]

Treatment of FaO rat hepatoma cells with TGF-beta selects cells that survive to its apoptotic effect and undergo epithelial-mesenchymal transitions (EMT). We have established a cell line (T beta T-FaO, from TGF-beta-treated FaO) that shows a mesenchymal, de-differentiated, phenotype in the presence of TGF-beta and is refractory to its suppressor effects. In the absence of this cytokine, cells revert to an epithelial phenotype in 3-4 weeks and recover the response to TGF-beta. T beta T-FaO show higher capacity to migrate than that observed in the parental FaO cells. We found that FaO cells express low levels of CXCR4 and do not respond to SDF-1 alpha. However, TGF-beta up-regulates CXCR4, through a NF kappaB-dependent mechanism, and T beta T-FaO cells show elevated levels of CXCR4, which is located in the presumptive migration front. A specific CXCR4 antagonist (AMD3100) attenuates the migratory capacity of T beta T-FaO cells on collagen gels. Extracellular SDF-1 alpha activates the ERKs pathway in T beta T-FaO, but not in FaO cells, increasing cell scattering and protecting cells from apoptosis induced by serum deprivation. Targeted knock-down of CXCR4 with specific siRNA blocks the T beta T-FaO response to SDF-1 alpha. Thus, the SDF-1/CXCR4 axis might play an important role in mediating cell migration and survival after a TGF-beta-induced EMT in hepatoma cells.

Place, publisher, year, edition, pages
2009. Vol. 21, no 11, p. 1595-1606
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Basic Medicine
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URN: urn:nbn:se:uu:diva-339279DOI: 10.1016/j.cellsig.2009.06.006PubMedID: 19586611OAI: oai:DiVA.org:uu-339279DiVA, id: diva2:1175318
Available from: 2018-01-17 Created: 2018-01-17 Last updated: 2018-02-15Bibliographically approved

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