Objectives: To investigate the effects of intracellular calcium (Ca2+) mobilization, β-catenin and Akt signal pathways after the binding of metastatic ovarian cells to fibronectin.
Materials and methods: The expression levels of α4β1 and αvβ6 integrin were determined using α4, β1, αv, and β6 antibodies using flow cytometry on PEO-1 cells. The effect of [Ca2+]i on cell adhesion capacity was investigated using RTCA after stimulating PEO-1 cells using thapsigargin and tunicamycin. The binding rate of PEO-1 cells to fibronectin was also investigated in the presence of either different concentrations of cardamonin, which inhibits the accumulation of β-catenin, or different concentrations of FPA 124, which is a specific inhibitor for the PKB/Akt signal pathway, using RTCA.
Results: RTCA analysis results showed that increasing [Ca2+]i through leakage of the calcium pool was strongly effective on PEO-1 cell binding to fibronectin. Extracellular calcium influx also reduced the binding of PEO-1 cells. Cell binding to fibronectin was also inhibited with a ratio of 64% in the presence of 100 µM cardamonin compared with untreated control cells. Finally, it was found that PKB/Akt inhibition with 15 µM FPA 124 decreased the binding of PEO-1 cells to fibronectin with a ratio of 88% compared with untreated control cells.
Conclusion: PEO-1 cell binding to fibronectin via integrins could be related to intracellular Ca2+ mobilization and Akt signaling.
Keywords: Fibronectin; calcium; ovarian cancer; tunicamycin.
©Copyright 2018 Turk J Pharm Sci, Published by Galenos Publishing House.