LPA receptor activation induces PKCα nuclear translocation in glioblastoma cells.

Lysophosphatidic acid (LPA) is a ubiquitous lysophospholipid that induces a wide range of cellular processes such as wound healing, differentiation, proliferation, migration, and survival. LPA signaling is increased in a number of cancers. In Glioblastoma (GBM), the most aggressive brain tumor, autotaxin the enzyme that produces LPA and its receptor LPA are overexpressed. LPA is preferentially couple to Gα proteins in these tumors that in turn activates PKCs. PKCs are involved in many cellular processes including proliferation and metastasis. In this study, we aimed to determine if a classical PKC (α isozyme), could be activated through LPA in GBM cell lines and if this activation impacts on cell number. We found that LPA induces PKCα translocation to the nucleus, but not to the cell membrane after LPA treatment and the cell number diminished when LPA/PKCα signaling was blocked, suggesting a relevant role of LPA and PKCα in GBM growth.