Figure S3.

Peripheral ruffling, invadopodia formation, and gelatin degradation in MAP1B-depleted MDA-MB-231, BT549, and Hs578T cells. (A) Kymograph of cortactin-positive peripheral ruffling in mock and MAP1B siRNA-transfected MDA/cortactin-GPF cells. (B and C) Upper panel: Cortactin/actin-positive invadopodia (B) and extracellular gelatin degradation (C) in MAP1B shRNA-based stable KD MDA-MB-231 cells. Lower panel: Quantification of cells with cortactin/actin-positive invadopodia (B) and extracellular gelatin degradation (C). (D and E) Upper panel: Cortactin/actin-positive invadopodia (D) and extracellular gelatin degradation (E) in MAP1B CRISPR/Cas9-based KO MDA-MB-231 cells. Lower panel: Quantification of cells with cortactin/actin-positive invadopodia (D) and extracellular gelatin degradation (E). (F) Cortactin/actin-positive invadopodia in MAP1B siRNA-based transient KD BT549 (upper) and Hs578T (lower) cells. (G) Extracellular gelatin degradation in MAP1B siRNA-based transient KD BT549 (upper) and Hs578T (lower) cells. (B–E) The values indicate the mean ± SEM. B, n = 4 experiments; C–E, n = 3 experiments. P values were determined using one-way ANOVA with Dunnett’s multiple comparison test. **, P < 0.01; ***, P < 0.001. Scale bars, 10 μm.

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