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Spatiotemporally Controlled Nuclear Translocation of Guests in Living Cells Using Caged Molecular Glues as Photoactivatable Tags
Published on: January 17, 2019
LPA1 receptor activation induces PKCα nuclear translocation in glioblastoma cells
Silvia Anahi Valdés-Rives1, Marisol de la Fuente-Granada1, Marco A Velasco-Velázquez2
1Departamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad de México, Mexico.
Abstract:
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.
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