Supplementary Figures S1-S17 from Dynamic Glycoprotein Hyposialylation Promotes Chemotherapy Evasion and Metastatic Seeding of Quiescent Circulating Tumor Cell Clusters in Breast Cancer

Supplementary Figure S1-S17 show the methods of CTC analysis and CTC-associated survival (S1); glycosylation profiles of patient CTCs (S2); phenotypic effects of neuraminidase treatment and CD44 depletion on tumor clustering and sialylation (S3); N-glycomic analysis of α2,6-SA peaks in WT and ST6KO cells (S4); Depletion of ST6GAL1 or ST3GAL1 promotes clustering and chemo-evasion (S5); ST6GAL1 expression and cell sensitivity to therapeutics (paclitaxel, doxorubicine and palbociclib) (S6); he altered gene pathways in ST6GAL1-KO cells (S7); ST6GAL1 is associated with cell growth and patient survival (S8); dynamic glycosylation profile in PDXs and breast tumors (S9); ST6GAL1 suppresses metastatic seeding (S10); Counts and Ki67 expression of CTCs and DTCs in situ (S11); depletion of ST6GAL1 promotes transendothelial migration and seeding (S12); α2,6-sialylation of CD44 by ST6GAL1 (S13); ST6GAL1 substrates regulate cluster formation via altered binding affinity (S14); the down-regulation of ST6GAL1 substrates inhibits metastatic seeding (S15); anti-PODXL inhibits tumor cell cluster formation and metastatic seeding (S16); and anti-PODXL effects on CTCs and seeding of PDX-M1 (S17).