IQUIFIB   02644
INSTITUTO DE QUIMICA Y FISICOQUIMICA BIOLOGICAS "PROF. ALEJANDRO C. PALADINI"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Concomitant mitogenic effects of growth hormone and epidermal growth factor over MCF7 cancer cells
Autor/es:
GÁNDOLA YB; WOELKER V; IRENE PE; SOTELO AI; MIQUET JG; TURYN D; GONZALEZ L
Lugar:
Ciudad de Buenos Aires
Reunión:
Congreso; XLIXI Reunión Anual de la Sociedad Argentina de Investigación Bioquímica y Biología Molecular (SAIB); 2013
Institución organizadora:
XLIXI Reunión Anual de la Sociedad Argentina de Investigación Bioquímica y Biología Molecular (SAIB
Resumen:
Concomitant mitogenic effects of growth hormone and epidermal growth factor over MCF7 cancer cells   Gándola YB, Woelker V, Irene PE, Sotelo AI, Miquet JG, Turyn D, Gonzalez L. Instituto de Química y Fisicoquímica Biológica, Facultad de Farmacia y Bioquímica, UBA, Argentina. Growth hormone (GH) is essential for normal growth and development of the mammary gland. However, high GH levels were associated with pathogenesis and progression of breast cancer. GH modulates epidermal growth factor receptor (EGFR) expression and signaling, broadly involved in cancer pathogenesis, in cell types different from the breast tissue. In this study, we explored the crosstalk between GH and EGF signaling pathways in the epithelial breast cancer cell line MCF-7 to understand how these factors might work together to affect breast cancer behavior. For this purpose, EGFR expression and signalling were assessed in MCF-7 cells after incubation with GH, EGF or both and results were correlated with effects on proliferation. These studies showed that concomitant treatment with GH and EGF during two hours inhibits ligand-induced EGFR downregulation. GH did not synergize with EGF in activating Erk1/2 or Akt; on the contrary, Erk1/2 activation by concomitant treatment with GH and EGF was diminished respect to the addition of their individual effects. Such desensitization was associated with reduced induction of cyclin D1 expression and proliferation of cells treated with GH and EGF. In conclusion, inhibition of ligand-induced EGFR downregulation by GH co-treatment would attenuate Erk1/2 activation, cyclin D1 induction and promotion of cell proliferation of the breast cancer cells.