Skip to main content
Fig. 3 | Breast Cancer Research

Fig. 3

From: Vangl-dependent Wnt/planar cell polarity signaling mediates collective breast carcinoma motility and distant metastasis

Fig. 3

Wnt/PCP signaling drives collective cell invasion ex vivo and is upregulated in the K14-positive leader cell population. a Representative bright field images of MMTV-PyMT-derived mouse mammary tumor organoids stably overexpressing Vector, Vangl1, Vangl2 or Wnt5a invading into collagen in the presence of 2.5 nm bFGF, scale bars = 50 µm. b Quantification of the percentage of organoids counted with 0–2, 3–5, and 6 + collectively invading protrusions for Vector-, Vangl1-, Vangl2-, or Wnt5a-expressing organoids (Vector n = 547, Vangl1 n = 371, Vangl2 n = 276, Wnt5a n = 456 organoids counted from six independent experiments, p values represent Vector (V) vs Vangl1 (V1), Vangl2 (V2), Wnt5a (W), 0–2 protrusions; V vs V1 p = 0.0011, V vs V2 p = 6.32E-06, V vs W p = 2.50E-05, 3–5 protrusions; V vs V1 p = 0.0001, V vs V2 p = 8.94E-05, V vs W p = 0.0092, 6 + protrusions; V vs V1 p = 0.0027, V vs V2 p = 0.0132, V vs W p = 0.0024). Bar graphs represent the mean ± sem of experimental replicates (n), significance was determined by a two-sided unpaired t test, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. c Analysis of RNA-sequencing data set SRP066316 from NCBI Sequence Read Archive for Wnt5a, Vangl2, and Vangl1 transcript in K14- and K14 + cells derived from MMTV-PyMT tumors (Wnt5a p = 7.15E-05, Vangl2 p = 0.0049, VANGL1 p = 0.0422), significance was determined by likelihood ratio test followed by Benjamin–Hochberg correction for multiple hypothesis testing

Back to article page