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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: O-GlcNAcylation homeostasis controlled by calcium influx channels regulates multiple myeloma dissemination

Fig. 5

Hyper-O-GlcNAcylation suppresses MM cell motility via ITGA4 and ITGB7. a Human MM-derived RPMI8226 cells were treated with various concentrations of thiamet G (0–10 μM) and analyzed for cell adhesion proteins, including ITGB1, ITGB3, ITGB7, ITGA4, ITGA5, ITGAV, E-cad, N-cad, and B-cat by Western blotting. b Quantitative analysis of the indicated proteins, normalized to β-actin and relative to the non-treated cells (NTX) (see also Additional file 2: Fig. S19 for an additional quantification). Data mean ± SD (n = 4). *P < 0.05, **P < 0.01, ***P < 0.001 versus NTX; two-tailed Student’s t-test. c ITGA4 and ITGB7 expression in MM tissues in comparison to NPC in a clinical dataset available on Oncomine™ bioinformatics database. Data mean ± SD. *P < 0.05, ***P < 0.001 versus NPC; two-tailed Student’s t-test. d, e OGA-knockdown sgMGEA5 RPMI8226 and NCI-H929 cells were evaluated for ITGA4 and ITGB7 levels by Western blotting to confirm that they are downstream of O-GlcNAcylation. (lower) Quantitative analysis of ITGA4 and ITGB7 levels, normalized to β-actin and relative to WT control cells. Data mean ± SD. ***P < 0.001 versus WT; two-tailed Student’s t-test

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