Objective: To detect the role of ERK in the hormesis induced by cadmium chloride in HEK293 cells.
Methods: HEK293 cells were treated with CdCl2 of 0, 0.0005, 0.005, 0.05, 0.5, 5, 50, 500 micromol/L for 12h and 24h. The ERK inhibitors (PD98059, U0126) and c-raf shRNA were added before the cell was treated with CdCl2. The proliferation viability was measured by thethiazolyl blue (MTT) and WST-8 assay. The level of the phosphorylated ERK and c-raf was examined with the western blot method. The level of c-fos, c-myc and c-raf mRNA was examined with RT-PCR.
Results: CdCl2 stimulated cell proliferation at lower concentrations (0.05 and 0.5 micromol/L) but inhibit it at higher concentrations (50 and 500 micromol/L). The c-fos mRNA increased significantly at low concentrations (0.51 micromol/L) and the c-myc mRNA increased with CdCl2 concentration. Treated with 100 micromol/L ERK1/2 inhibitor and c-raf shRNA, the cell proliferation did not increase significantly at low concentrations (0.05 and 0.51 micromol/L), but still decreased at high concentrations (50 and 500 micromol/L).
Conclusion: CdCl2 can induce the hormesis of HEK293 cell proliferation. The c-fos of ERK pathway may be involved in the biphasic effect induced by CdCl2.
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