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Antitumour effects of PLC-γ1-(SH2)2-TAT fusion proteins on EGFR/c-erbB-2-positive breast cancer cells

Katterle, Y ; Brandt, B H ; Dowdy, S F ; Niggemann, B ; Zänker, K S ; Dittmar, T

British journal of cancer, 2004-01, Vol.90 (1), p.230-235 [Periódico revisado por pares]

Nature Publishing Group

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  • Título:
    Antitumour effects of PLC-γ1-(SH2)2-TAT fusion proteins on EGFR/c-erbB-2-positive breast cancer cells
  • Autor: Katterle, Y ; Brandt, B H ; Dowdy, S F ; Niggemann, B ; Zänker, K S ; Dittmar, T
  • Assuntos: Experimental Therapeutics
  • É parte de: British journal of cancer, 2004-01, Vol.90 (1), p.230-235
  • Descrição: Due to its pivotal role in the growth factor-mediated tumour cell migration, the adaptor protein phospholipase C- γ 1 (PLC- γ 1) is an appropriate target to block ultimately the spreading of EGFR/c-erbB-2-positive tumour cells, thereby minimising metastasis formation. Here, we present an approach to block PLC- γ 1 activity by using protein-based PLC- γ 1 inhibitors consisting of PLC- γ 1 SH2 domains, which were fused to the TAT-transduction domain to ensure a high protein transduction efficiency. Two proteins were generated containing one PLC- γ 1-SH2-domain (PS1-TAT) or two PLC- γ 1-SH2 domains (PS2-TAT). PS2-TAT treatment of the EGFR/c-erbB-2-positive cell line MDA-HER2 resulted in a reduction of the EGF-mediated PLC- γ 1 tyrosine phosphorylation of about 30%, concomitant with a complete abrogation of the EGF-driven calcium influx. In addition to this, long-term PS2-TAT treatment both reduces the EGF-mediated migration of about 75% combined with a markedly decreased time locomotion of single MDA-HER2 cells as well as decreases the proliferation of MDA-HER2 cells by about 50%. Due to its antitumoral capacity on EGFR/c-erbB-2-positive breast cancer cells, we conclude from our results that the protein-based PLC- γ 1 inhibitor PS2-TAT may be a means for novel adjuvant antitumour strategies to minimise metastasis formation because of the blockade of cell migration and proliferation.
  • Editor: Nature Publishing Group
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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