13058_2020_1245_MOESM10_ESM.pdf (9.21 MB)
MOESM10 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 10: Figure S10. AMPK activation is not appreciably regulated by p66ShcA 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 pAMPK and AMPK specific antibodies. Percentage of pAMPK positive pixels in primary breast tumors (n = 7–8 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 = 214 lesions; p66-CR (WT), n = 194 lesions; p66-CR (S36A), n = 202 lesions. (B, C) Representative IHC images for primary breast tumors and lung metastases are shown.
