Skip to main content
. 2021 Apr 13;12:2198. doi: 10.1038/s41467-021-22522-4

Fig. 5. EFA6B knock-out induces the expression of EMT transcription factors that promote collective invasion of MCF10A and HMLE WT cells in collagen I.

Fig. 5

a The MCF10A WT, the homozygous EFA6B KO55, KO50, KO2, and the heterozygous EFA6B KO2.9 (Het2.9) cells were solubilized and the expression of the indicated proteins analyzed by immunoblot. Actin served as a loading control. N = 3. Quantification is shown in Supplementary Fig. 3f. b Expression of EMT-associated genes by qPCR analysis in EFA6B KO55 cells normalized to MCF10A WT. N = 3, average ± SEM. c The HMLE WT population, the luminal progenitor clone WT23, heterozygous KO25, homozygous KO3, and the mature basal clone WT4, homozygous KO1 cells were solubilized and the expression of the indicated proteins analyzed by immunoblot. Actin served as a loading control. N = 3. Quantification is shown in Supplementary Fig. 3f. d Expression of EMT-TF genes by qPCR analysis in EFA6B KO3 and KO1 cells normalized to their respective HMLE control cells WT23 and WT4. N = 3, average ± SD. e Quantification of the percentage of aggregates (n = 100) with invasive protrusions of MCF10A KO55 cells grown in collagen I for 2 days after transfection with the indicated siRNAs. N = 3, average ± SEM, one-way ANOVA test with Dunnett’s multiple comparison p-values. f Quantification of the percentage of aggregates (n = 100) with invasive protrusions of HMLE KO3 (left) and KO1 (right) cells grown in collagen I for 2 days after transfection with the SNAIL1 targeted siRNAs. N = 3, average ± SEM, one-way ANOVA test with Dunnett’s multiple comparison p-values. Source data are provided as a Source Data file.