In sum, our results propose the following hypothetical model of NMU's oncogenic role in dependency of NMUR2 expression in breast cancer: crosstalk of NMU signaling with several cancer-relevant pathways, e.g. WNT, TGFβ and ERK cascade results in decreased expression of the canonical WNT target MYC and enhanced activation of the non-canonical WNT/planar cell polarity (PCP) pathway effector RAC1 among others, possibly contributing to growth inhibition and promotion of cell migration (Figure 8D). Here, TGFB1 is linked to breast cancer.