Lysophosphatidic acid (LPA) signaling via LPA receptors (LPA to LPA) regulates a variety of malignant properties of cancer cells. It is known that endothelial cells promote tumor progression and chemoresistance. The present study aimed to investigate the roles of LPA in cellular functions modulated by endothelial cells and anticancer drug in osteosarcoma cells. Human osteosarcoma MG-63 cells were maintained in endothelial F2 cell supernatants. After culturing for 3 months, MG63-F2 cells were established. LPAR5 expression level in MG63-F2 cells was significantly elevated, compared with MG-63 cells. The cell motile activity of MG63-F2 cells was markedly higher than that of MG-63 cells. To validate the effects of LPA on cell motile activity, LPA knockdown cells were generated from MG-63 cells. The cell motile activity of MG-63 cells was inhibited by LPA knockdown. The cell survival to cisplatin (CDDP) was reduced in MG-63 cells treated with LPA. In the presence of LPA, the cell survival rate was significantly lower in MG63-F2 cells than MG-63 cells, correlating with LPAR5 expression. LPA knockdown cells indicated the high cell survival rate to CDDP. Moreover, LPAR5 expression level was increased in the long-term CDDP treated MG63-C cells. The cell survival to CDDP of MG63-C cells was enhanced by LPA knockdown. These results suggest that cellular functions are regulated through LPA-mediatd signaling induced by endothelial cells and CDDP in MG-63 cells.
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| http://dx.doi.org/10.1016/j.yexcr.2020.111813 | DOI Listing |
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