Akt Interaction with PLCγ Regulates the G2/M Transition Triggered by FGF Receptors from MDA-MB-231 Breast Cancer Cells

Background/Aim: Estrogen-independent breast cancer cell growth is under the control of fibroblast growth factors receptors (FGFRs), but the role of phospholipase C gamma (PLCγ) and Akt, the downstream effectors activated by FGFRs, in cell proliferation is still unresolved. Materials and Methods: FG...

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Published in:Anticancer research 2009-12, Vol.29 (12), p.4965
Main Authors: EDITH BROWAEYS-POLY, DOMINIQUE PERDEREAU, ARLETTE LESCUYER, ANNE-FRANÇOISE BURNOL, KATIA CAILLIAU
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container_issue 12
container_start_page 4965
container_title Anticancer research
container_volume 29
creator EDITH BROWAEYS-POLY
DOMINIQUE PERDEREAU
ARLETTE LESCUYER
ANNE-FRANÇOISE BURNOL
KATIA CAILLIAU
description Background/Aim: Estrogen-independent breast cancer cell growth is under the control of fibroblast growth factors receptors (FGFRs), but the role of phospholipase C gamma (PLCγ) and Akt, the downstream effectors activated by FGFRs, in cell proliferation is still unresolved. Materials and Methods: FGFRs from highly invasive MDA-MB-231 cells were expressed in Xenopus oocyte, a powerful model system to assess the G 2 /M checkpoint regulation. Under FGF1 stimulation, an analysis of the progression in the M-phase of the cell cycle and of the Akt signaling cascades were performed using the phosphatidylinositol-3-kinase inhibitor, LY294002, and a mimetic peptide of the SH3 domain of PLCγ. Results: Activated Akt binds and phosphorylates PLCγ before Akt targets the tumor suppressor Chfr. Disruption of the Akt-PLCγ interaction directs Akt binding to Chfr and accelerates the alleviation of the G 2 /M checkpoint. Conclusion: The PLCγ-Akt interaction, triggered by FGF receptors from estrogen-independent breast cancer cells MDA-MB-231, regulates progression in the M-phase of the cell cycle.
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Materials and Methods: FGFRs from highly invasive MDA-MB-231 cells were expressed in Xenopus oocyte, a powerful model system to assess the G 2 /M checkpoint regulation. Under FGF1 stimulation, an analysis of the progression in the M-phase of the cell cycle and of the Akt signaling cascades were performed using the phosphatidylinositol-3-kinase inhibitor, LY294002, and a mimetic peptide of the SH3 domain of PLCγ. Results: Activated Akt binds and phosphorylates PLCγ before Akt targets the tumor suppressor Chfr. Disruption of the Akt-PLCγ interaction directs Akt binding to Chfr and accelerates the alleviation of the G 2 /M checkpoint. 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title Akt Interaction with PLCγ Regulates the G2/M Transition Triggered by FGF Receptors from MDA-MB-231 Breast Cancer Cells
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