Overexpression of NmU also resulted in upregulation of epithelial-mesenchymal transition markers and increased IL-6 secretion which, together with aberrant metabolism, have all been associated with the cancer stem cell (CSC) phenotype.
Although NmU exerted no effects on cancer cell proliferation, it induced c-Met and a trend towards increased invasiveness as well as an increased hepatocyte growth factor (HGF)-mediated scattering.
In conclusion, NMU is a RhoGDI2-regulated gene that appears important for tumorigenicity, lung metastasis and cancer cachexia, and thus a promising therapeutic target in cancer.