INVESTIGADORES
CORTÉS MarÍa Alicia
congresos y reuniones científicas
Título:
Epidermal growth factor (EGF) partly compensates the lack of FAK and SHP-1 during PC3 cell migration
Autor/es:
JAVIER RODRIGUEZ-UBREVA; ARIEL E. CARIAGA-MARTINEZ; M. ALICIA CORTÉS; PILAR LÓPEZ-RUIZ; BEGOÑA COLÁS
Lugar:
Vienna
Reunión:
Congreso; 32nd FEBS Molecular Machines; 2007
Institución organizadora:
Febs
Resumen:
It is well known that metastasis is the cause of morbidity and mor-
tality in patients with cancer. Prostate cancer cells have a propen-
sity to metastasize to bone. This metastatic process is partly
controlled by tyrosine kinases and tyrosine phosphatases and
results from complex interactions between epithelium, stroma and
multiple growth factors. Thus, we analyzed the role of tyrosine
phosphatase SHP-1, tyrosine kinase FAK and epidermal growth
factor (EGF) in the regulation of cellular adhesion and migration
on collagen type I, the major bone extracellular matrix component.
Our results show that in human prostatic PC3 cancer cells, SHP-1
colocalizes with FAK in membrane lamellipodia, both proteins
being constitutively associated during cell adhesion and spreading
on collagen type I. Furthermore, the decrease of SHP-1 or FAK
expression by siRNA reduces basal cell transmigration, but poten-
ciates EGF-induced transmigration, coinciding with an up-regula-
tion of EGFR downstream signalling pathways, such as PI3K/Akt
and p44/42. In summary, our observations suggest the possible
existence of a mechanism in which EGF would partly compensate
the reduction of FAK or SHP-1 during the cell migration process.
This compensative mechanism could be due to a negative modula-
tion by FAK via SHP-1, in the EGFR pathway.