9-hydroxystearic acid (9HSA) induces cell proliferation arrest in G0/G1 by inhibiting HDAC1 and inducing p21 expression. Serum-starved cells are known to exit G1 and enter the G0 phase, but treatment with either serum or specific growth factors induces them to reenter the cycle. On the contrary, 9HSA treated cells, if stimulated with EGF, are not responsive and undergo a further arrest. In the effort of understanding the possible mechanisms of this effect we analysed the degree of internalisation of the EGF/EGFR complex and the interactions between the complex and other proteins, such as HDAC1 and pRb. The phosphorilation level of EGFR was indicative of its activity in the cells. Cyclin D1 promotor being one of the most important EGF/EGFR target involved in cell proliferation, we also analysed its expression, complexation, and localization with HDAC1.

9-HYDROXYSTEARIC ACID INTERFERES WITH EGF SIGNALLING IN A HUMAN COLON ADENOCARCINOMA

CALONGHI, NATALIA;TOGNOLI, CRISTINA;PAGNOTTA, ELEONORA;BOGA, CARLA;MASOTTI, LANFRANCO
2005

Abstract

9-hydroxystearic acid (9HSA) induces cell proliferation arrest in G0/G1 by inhibiting HDAC1 and inducing p21 expression. Serum-starved cells are known to exit G1 and enter the G0 phase, but treatment with either serum or specific growth factors induces them to reenter the cycle. On the contrary, 9HSA treated cells, if stimulated with EGF, are not responsive and undergo a further arrest. In the effort of understanding the possible mechanisms of this effect we analysed the degree of internalisation of the EGF/EGFR complex and the interactions between the complex and other proteins, such as HDAC1 and pRb. The phosphorilation level of EGFR was indicative of its activity in the cells. Cyclin D1 promotor being one of the most important EGF/EGFR target involved in cell proliferation, we also analysed its expression, complexation, and localization with HDAC1.
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N. Calonghi; C. Tognoli; E. Pagnotta; C. Boga; L. Masotti
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11585/9384
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