Supplemental Tables and Figures from EGFR Signaling Enhances Aerobic Glycolysis in Triple-Negative Breast Cancer Cells to Promote Tumor Growth and Immune Escape
crossref(2023)
Supplementary Table 1. Relationships between expression of p-PKM2, EGFR and Ki-67 in surgical specimens of triple-negative breast cancer patients. Supplementary Table 2. Relationships between expression of p-PKM2, EGFR and Ki-67 in surgical specimens of non-triple-negative breast cancer patients. Supplementary Figure S1. EGF signaling enhances aerobic glycolysis in TNBC cells. Supplementary Figure S2. PKM2 is a novel binding partner of EGFR and its activity is inhibited by EGFR via Tyr phosphorylation. Supplementary Figure S3. EGFR reprograms cancer cell metabolism by PKM2 phosphorylation in TNBC cells. Supplementary Figure S4. Upregulation of HK2 expression by EGF signaling also contributes to aerobic glycolysis in TNBC cells. Supplementary Figure S5. Glycolysis metabolite, F1,6BP, binds directly to and enhances the activity of EGFR. Supplementary Figure S6. The combination of EGFR and glycolysis inhibitors synergistically suppresses TNBC cell proliferation. Supplementary Figure S7. EGF signaling-induced lactate inhibits cytotoxic T cell activity in TNBC cells.