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Association of RHAMM with E2F1 promotes tumour cell extravasation by transcriptional up-regulation of fibronectin
The Journal of pathology, 2014-11, Vol.234 (3), p.351-364
Meier, Claudia
Spitschak, Alf
Abshagen, Kerstin
Gupta, Shailendra
Mor, Joel M.
Wolkenhauer, Olaf
Haier, Jörg
Vollmar, Brigitte
Alla, Vijay
Pützer, Brigitte M.
2014
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Meier, Claudia
Spitschak, Alf
Abshagen, Kerstin
Gupta, Shailendra
Mor, Joel M.
Wolkenhauer, Olaf
Haier, Jörg
Vollmar, Brigitte
Alla, Vijay
Pützer, Brigitte M.
Titel
Association of RHAMM with E2F1 promotes tumour cell extravasation by transcriptional up-regulation of fibronectin
Ist Teil von
The Journal of pathology, 2014-11, Vol.234 (3), p.351-364
Ort / Verlag
Chichester, UK: John Wiley & Sons, Ltd
Erscheinungsjahr
2014
Quelle
Wiley Online Library All Journals
Beschreibungen/Notizen
Dissemination of cancer cells from primary to distant sites is a complex process; little is known about the genesis of metastatic changes during disease development. Here we show that the metastatic potential of E2F1‐dependent circulating tumour cells (CTCs) relies on a novel function of the hyaluronan‐mediated motility receptor RHAMM. E2F1 directly up‐regulates RHAMM, which in turn acts as a co‐activator of E2F1 to stimulate expression of the extracellular matrix protein fibronectin. Enhanced fibronectin secretion links E2F1/RHAMM transcriptional activity to integrin‐β1–FAK signalling associated with cytoskeletal remodelling and enhanced tumour cell motility. RHAMM depletion abolishes fibronectin expression and cell transmigration across the endothelial layer in E2F1‐activated cells. In a xenograft model, knock‐down of E2F1 or RHAMM in metastatic cells protects the liver parenchyma of mice against extravasation of CTCs, whereas the number of transmigrated cells increases in response to E2F1 induction. Expression data from clinical tissue samples reveals high E2F1 and RHAMM levels that closely correlate with malignant progression. These findings suggest a requirement for RHAMM in late‐stage metastasis by a mechanism involving cooperative stimulation of fibronectin, with a resultant tumourigenic microenvironment important for enhanced extravasation and distant organ colonization. Therefore, stimulation of the E2F1–RHAMM axis in aggressive cancer cells is of high clinical significance. Targeting RHAMM may represent a promising approach to avoid E2F1‐mediated metastatic dissemination. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Sprache
Englisch
Identifikatoren
ISSN: 0022-3417
eISSN: 1096-9896
DOI: 10.1002/path.4400
Titel-ID: cdi_proquest_miscellaneous_1610759518
Format
–
Schlagworte
Animals
,
Blotting, Western
,
Cell Line, Tumor
,
Chromatin Immunoprecipitation
,
docking analyses
,
E2F1 transcription factor
,
E2F1 Transcription Factor - metabolism
,
Enzyme-Linked Immunosorbent Assay
,
Extracellular Matrix Proteins - metabolism
,
extravasation
,
feed-forward loop
,
fibronectin
,
Fibronectins - biosynthesis
,
Fluorescent Antibody Technique
,
Gene Expression Regulation, Neoplastic - physiology
,
Heterografts
,
human tissues
,
Humans
,
Hyaluronan Receptors - metabolism
,
Immunoprecipitation
,
Mice
,
Neoplasm Invasiveness - physiopathology
,
Neoplastic Cells, Circulating - metabolism
,
Reverse Transcriptase Polymerase Chain Reaction
,
RHAMM
,
Transcription, Genetic
,
Up-Regulation
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