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Sökning: onr:"swepub:oai:DiVA.org:uu-339268" > Overactivation of t...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003748naa a2200421 4500
001oai:DiVA.org:uu-339268
003SwePub
008180117s2013 | |||||||||||000 ||eng|
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3392682 URI
0247 a https://doi.org/10.1002/hep.265972 DOI
040 a (SwePub)uu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Bertran, Esther4 aut
2451 0a Overactivation of the TGF-β pathway confers a mesenchymal-like phenotype and CXCR4-dependent migratory properties to liver tumor cells
264 c 2013-10-11
264 1b Ovid Technologies (Wolters Kluwer Health),c 2013
338 a print2 rdacarrier
520 a UNLABELLED: Transforming growth factor-beta (TGF-β) is an important regulatory suppressor factor in hepatocytes. However, liver tumor cells develop mechanisms to overcome its suppressor effects and respond to this cytokine by inducing other processes, such as the epithelial-mesenchymal transition (EMT), which contributes to tumor progression and dissemination. Recent studies have placed chemokines and their receptors at the center not only of physiological cell migration but also of pathological processes, such as metastasis in cancer. In particular, CXCR4 and its ligand, stromal cell-derived factor 1α (SDF-1α) / chemokine (C-X-C motif) ligand 12 (CXCL12) have been revealed as regulatory molecules involved in the spreading and progression of a variety of tumors. Here we show that autocrine stimulation of TGF-β in human liver tumor cells correlates with a mesenchymal-like phenotype, resistance to TGF-β-induced suppressor effects, and high expression of CXCR4, which is required for TGF-β-induced cell migration. Silencing of the TGF-β receptor1 (TGFBR1), or its specific inhibition, recovered the epithelial phenotype and attenuated CXCR4 expression, inhibiting cell migratory capacity. In an experimental mouse model of hepatocarcinogenesis (diethylnitrosamine-induced), tumors showed increased activation of the TGF-β pathway and enhanced CXCR4 levels. In human hepatocellular carcinoma tumors, high levels of CXCR4 always correlated with activation of the TGF-β pathway, a less differentiated phenotype, and a cirrhotic background. CXCR4 concentrated at the tumor border and perivascular areas, suggesting its potential involvement in tumor cell dissemination.CONCLUSION: A crosstalk exists among the TGF-β and CXCR4 pathways in liver tumors, reflecting a novel molecular mechanism that explains the protumorigenic effects of TGF-β and opens new perspectives for tumor therapy.
650 7a NATURVETENSKAPx Biologi0 (SwePub)1062 hsv//swe
650 7a NATURAL SCIENCESx Biological Sciences0 (SwePub)1062 hsv//eng
7001 a Crosas-Molist, Eva4 aut
7001 a Sancho, Patricia4 aut
7001 a Caja, Laiau Bellvitge Biomedical Research Institute (IDIBELL), L’Hospitalet de Llobregat, Barcelona, Spain4 aut0 (Swepub:uu)laica659
7001 a Lopez-Luque, Judit4 aut
7001 a Navarro, Estanislao4 aut
7001 a Egea, Gustavo4 aut
7001 a Lastra, Raquel4 aut
7001 a Serrano, Teresa4 aut
7001 a Ramos, Emilio4 aut
7001 a Fabregat, Isabel4 aut
7102 a Bellvitge Biomedical Research Institute (IDIBELL), L’Hospitalet de Llobregat, Barcelona, Spain4 org
7730 t Hepatologyd : Ovid Technologies (Wolters Kluwer Health)g 58:6, s. 2032-44q 58:6<2032-44x 0270-9139x 1527-3350
8564 u https://aasldpubs.onlinelibrary.wiley.com/doi/pdfdirect/10.1002/hep.26597
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-339268
8564 8u https://doi.org/10.1002/hep.26597

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