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. 2022 Oct 6;23(19):11887. doi: 10.3390/ijms231911887

Figure 6.

Figure 6

Complex crosstalk between CXCL12/CXCR4/ACKR3 and EGFR-HER2 pathways suggests shared mechanisms in signaling to the ERK cascade. MDA-MB-361 cells (ER+ and HER2+) were serum-starved and treated for 2 h with the indicated inhibitors for either CXCR4 (small-molecule compound AMD3100, nanobody V400), ACKR3 (nanobody VUN700), EGFR tyrosine kinase activity (AG1478), Gi protein (PTX) or Src kinase (PP2), as detailed in the Materials and Methods. Afterwards, cells were stimulated with 10 nM CXCL12, 100 ng/mL EGF, 20 ng/mL Heregulin or the indicated combinations for 2 min. ERK1/2 activation was assessed in cell lysates as above. Data are mean ± SEM of 2 independent experiments for VUN400 and 3–9 independent experiments for the remaining conditions. * p < 0.05, ** p < 0.01 or *** p < 0.001, comparing to stimulated cells without inhibitor treatment.