13058_2020_1245_MOESM1_ESM.pdf (9.21 MB)
MOESM1 of p66ShcA functions as a contextual promoter of breast cancer metastasis
journal contribution
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-SiegelAdditional file 1: Figure S1. Non-mitochondrial p66ShcA restrains metastatic progression in a luminal breast cancer model. (A) Immunoblot analysis of vector control (VC), p66ShcA-WT and p66ShcA-S36A overexpressing NIC cells using ShcA- and Tubulin-specific antibodies. (B) Mammary fat pad (MFP) injection of VC, p66ShcA-WT and p66ShcA-S36A overexpressing NIC cells. The data is shown as average tumor volume (mm3) ± SEM (n = 7 tumors/group). Immunohistochemical staining of the indicated mammary tumors using (C) Ki67 and (D) cleaved Caspase-3 specific antibodies. Representative images are shown. (E) Percentage of tumor burden in the lungs of mice bearing VC, p66ShcA-WT and p66ShcA-S36A overexpressing NIC tumors. Mammary tumors were resected at 500 mm3 and the development of lung metastases was quantified 28 days later. The data is shown as average lung tumor burden ±SEM (n = 9–12 mice/group). Representative images are shown. Statistical analysis was performed using a one-way Anova with a Tukey’s multiple comparisons test (*P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001).