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MOESM11 of p66ShcA functions as a contextual promoter of breast cancer metastasis

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posted on 2020-01-16, 04:56 authored by Kyle Lewis, Alex Kiepas, Jesse Hudson, Julien Senecal, Jacqueline Ha, Elena Voorand, Matthew Annis, Valerie Sabourin, Ryuhjin Ahn, Rachel Selva, Sébastien Tabariès, Brian Hsu, Matthew Siegel, Matthew Dankner, Eduardo Canedo, Mathieu Lajoie, Ian Watson, Claire Brown, Peter Siegel, Josie Ursini-Siegel
Additional file 11: Figure S11. Src family kinase activation is increased by non-mitochondrial p66ShcA pools in mammary tumors. (A) Whole cell lysates were generated from the indicated cell lines grown under the following conditions: 10% FBS versus 0% FBS for 16 h; 1 mM phenformin for 2 h; 20 μM sodium arsenate for 4 h; suspension cultures on ultra-low attachment plates for 16 h. Immunoblot analysis was performed using pSFK and Src specific antibodies. Percentage of pSFK positive pixels in primary breast tumors (n = 6–7 tumors/genotype) (B) and in individual lung-metastatic lesions (C) derived from 4T1-537 p66-CR (VC), p66-CR (WT) and p66-CR (S36A) breast cancer cells. For the lung metastases: p66-CR (VC), n = 318 lesions; p66-CR (WT), n = 308 lesions; p66-CR (S36A), n = 318 lesions. (B, C) Representative IHC images for primary breast tumors and lung metastases are shown. Statistical analysis performed using a one-way Anova with a Tukey’s multiple comparisons test (*P < 0.05).

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Canadian Institutes of Health Research

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