: Previous studies have shown that p21 (1) and histone hyperacetylation are important in basal growth inhibition by 9-HSA (2). It is known that serum-starved cells exit G1 and enter the G0 phase but can be induced to reenter the cell cycle through treatment with either serum or specific growth factors. We were therefore interested in determining whether colon cancer cells that had been withdrawn in the G0 phase of the cell cycle by treatment with 9-HSA were also capable of reentering the cell cycle after treatment with epidermal growth factor (EGF). Previous studies have shown that FAK is important in linking EGFR activation to the cellular machinery that promotes proliferation and cell migration (3). To determine wether 9-HSA treatment interferes with signal trasduction involving EGFR and FAK, we analyzed FAK expression and its phosphorylation levels, HT29 invasion index after EGF stimulation, in control and 9-HSA treated cells. Our data indicate that the treatment with 9-HSA induces a molecular phenotype characterized by a lack of growth factor responsiveness and diminished cell migration.
The EGF- induced cell proliferation and migration in HT29 is inhibited by 9-hydroxystearic acid
CALONGHI, NATALIA;PAGNOTTA, ELEONORA;CAPPADONE, CONCETTINA;BOGA, CARLA;MASOTTI, LANFRANCO
2004
Abstract
: Previous studies have shown that p21 (1) and histone hyperacetylation are important in basal growth inhibition by 9-HSA (2). It is known that serum-starved cells exit G1 and enter the G0 phase but can be induced to reenter the cell cycle through treatment with either serum or specific growth factors. We were therefore interested in determining whether colon cancer cells that had been withdrawn in the G0 phase of the cell cycle by treatment with 9-HSA were also capable of reentering the cell cycle after treatment with epidermal growth factor (EGF). Previous studies have shown that FAK is important in linking EGFR activation to the cellular machinery that promotes proliferation and cell migration (3). To determine wether 9-HSA treatment interferes with signal trasduction involving EGFR and FAK, we analyzed FAK expression and its phosphorylation levels, HT29 invasion index after EGF stimulation, in control and 9-HSA treated cells. Our data indicate that the treatment with 9-HSA induces a molecular phenotype characterized by a lack of growth factor responsiveness and diminished cell migration.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
