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LPA1 receptor activation induces PKCα nuclear translocation in glioblastoma cells
- Valdés-Rives, Silvia Anahi, de la Fuente-Granada, Marisol, Velasco-Velázquez, Marco A., González-Flores, Oscar, González-Arenas, Aliesha
- The international journal of biochemistry & cell biology 2019 v.110 pp. 91-102
- brain neoplasms, cell lines, cell membranes, glioblastoma, isozymes, metastasis, protein kinase C, proteins, tissue repair
- 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 LPA1 are overexpressed. LPA1 is preferentially couple to Gαq 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 LPA1 in GBM cell lines and if this activation impacts on cell number. We found that LPA1 induces PKCα translocation to the nucleus, but not to the cell membrane after LPA treatment and the cell number diminished when LPA1/PKCα signaling was blocked, suggesting a relevant role of LPA1 and PKCα in GBM growth.