LPA₁ 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 LPA₁ are overexpressed. LPA₁ is preferentially couple to Gα_q proteins in these tumors that in turn activates are involved in many cellular processes including proliferation and metastasis. In this study, we aimed to determine if a classical (α isozyme), could be activated through LPA₁ in GBM cell lines and if this activation impacts on cell number. We found that LPA₁ induces translocation to the nucleus, but not to the cell membrane after LPA treatment and the cell number diminished when signaling was blocked, suggesting a relevant role of LPA₁ and duanyu1531α in GBM growth.

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