MOESM10 of p66ShcA functions as a contextual promoter of breast cancer metastasis

Kyle Lewis, Alex Kiepas, Jesse Hudson, Julien Senecal, Jacqueline Ha, Elena Voorand, Matthew Annis, Valerie Sabourin, Ryuhjin Ahn, Rachel Selva, Sébastien Tabariès, Brian Hsu (+8 others)
2020 Figshare  
Additional 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
more » ... 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.
doi:10.6084/m9.figshare.11626602.v1 fatcat:rwq4senlojctlbah444zatod3m