Four phospholipase C β (PLCB) isoforms, PLCB1, PLCB2, PLCB3 and PLCB4, have been previously investigated regarding their roles in the metabolism of inositol lipids and cancer.
Using archival FFPE samples and DCIS-derived cells, we demonstrate that PLC-β2 is up-regulated in DCIS and that its forced down-modulation induces an epithelial-to-mesenchymal shift, expression of the cancer stem cell marker CD133, and the acquisition of invasive properties.
Up-modulation of PLC-β2 reduces the number and malignancy of triple-negative breast tumor cells with a CD133<sup>+</sup>/EpCAM<sup>+</sup> phenotype: a promising target for preventing progression of TNBC.
In addition, our data showing that the forced up-regulation of PLC-β2 counteracts the invasiveness of CD133-positive MDA-MB-231 cells might contribute to identify unexplored key steps responsible for the TNBC high malignancy, to be considered for potential therapeutic strategies.