| Literature DB >> 7541721 |
C L Hall1, B Yang, X Yang, S Zhang, M Turley, S Samuel, L A Lange, C Wang, G D Curpen, R C Savani, A H Greenberg, E A Turley.
Abstract
Overexpression of the RHAMM gene by transfection into fibroblasts is transforming and causes spontaneous metastases in the lung. H-ras-transformed fibrosarcomas transfected with a dominant suppressor mutant of RHAMM exhibit a so-called revertant phenotype and are completely nontumorigenic and nonmetastatic. Conversely, fibroblasts stably expressing low levels of RHAMM as a result of antisense transfection are resistant to ras transformation. Collectively, these results indicate that RHAMM acts downstream of ras. The loss of functional RHAMM ablates signaling within focal adhesions, in particular changes in focal adhesion kinase phosphorylation, and as a result these focal adhesions are unable to turn over in response to hyaluronan. These results provide evidence of the oncogenic potential of a novel extracellular matrix receptor and establish a functional link between transformation by ras and signaling within focal adhesions that are required for transformation by this oncogene.Entities:
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Year: 1995 PMID： 7541721 DOI： 10.1016/0092-8674(95)90048-9
Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 41.582