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. 2022 Jan 12;30(4):1536–1552. doi: 10.1016/j.ymthe.2022.01.017

Figure 4.

Figure 4

Pro-adhesive glycans on tumor cells with BZM-sensitive versus BZM-resistant adhesion

(A–D) Percentage changes of flow-resistant adhesions on cytokine-stimulated ECs as well as absolute changes in static E-selectin binding capacity and different tumor-cell-surface carbohydrate residue levels before and after indicated treatments of tumor cells from the different cell lines. (E) Human glycosyltransferase gene expression profiler array. (F) Differential protein levels of C2GNT2 in the indicated tumor cell lines. (G) Tumor-cell-surface sLeA/X expression and static E-selectin binding capacity after shRNA-mediated knock down of C2GNT2. The inserted box represents key glycosylation steps relevant to this study. Arrows in (A)–(D) highlight changes in E-selectin binding, sLeA expression, or β-1,6-GlcNAc (lectin PHA-L binding site) and poly-LacNAc (lectin DSL binding site) levels upon treatments. ND, neuraminidase; GOB, GalNAc-α-O-benzyl; SW, swainsonine; PHA-L, Phaseolus vulgaris leukoagglutinin; DSL, Datura stramonium lectin. Bar charts represent mean ± SD of three replicates; ∗p < 0.05