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Filamin A mediates HGF/c-MET signaling in tumor cell migration.

Artikel i vetenskaplig tidskrift
Författare Xianghua Zhou
Asli Toylu
Rajesh K. Nallapalli
Gisela M A Nilsson
Nese Atabey
Carl-Henrik Heldin
Jan Borén
Martin Bergö
Levent Akyürek
Publicerad i International journal of cancer. Journal international du cancer
Volym 128
Nummer/häfte 4
Sidor 839-846
ISSN 1097-0215
Publiceringsår 2011
Publicerad vid Wallenberglaboratoriet
Institutionen för biomedicin
Sidor 839-846
Språk en
Länkar dx.doi.org/10.1002/ijc.25417
Ämnesord migration; invasion; melanoma cells; fibroblasts
Ämneskategorier Kardiovaskulär medicin, Molekylär medicin (genetik och patologi)

Sammanfattning

Deregulated hepatocyte growth factor (HGF)/c-MET axis has been correlated with poor clinical outcome and drug resistance in many human cancers. Identification of novel regulatory mechanisms influencing HGF/c-MET signaling may therefore be necessary to develop more effective cancer therapies. In our study, we show that multiple human cancer tissues and cells express filamin A (FLNA), a large cytoskeletal actin-binding protein, and expression of c-MET is significantly reduced in human tumor cells deficient for FLNA. The FLNA-deficient tumor cells exhibited poor migrative and invasive ability in response to HGF. On the other hand, the anchorage-dependent and independent tumor cell proliferation was not altered by HGF. The FLNA-deficiency specifically attenuated the activation of the c-MET downstream signaling molecule AKT in response to HGF stimulation. Furthermore, FLNA enhanced c-MET promoter activity by its binding to SMAD2. The impact of FLNA deficiency on c-MET expression and HGF-mediated cell migration in human tumor cells was confirmed in primary mouse embryonic fibroblasts deficient for Flna. These data suggest that FLNA is one of the important regulators of c-MET signaling and HGF-induced tumor cell migration.

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