OBJECTIVE: To investigate the effect of cell proliferation in human breast cancer cells (MDA-MB 435), which has non-receptor of estrogen (Er), induced by beta-ionone. MDA-MB 435 cells were treated with different beta-ionone concentrations (25, 50, 100 and 200 micromol/L), with a negative control. METHODS: Such as curve of cell growth, cellular mitosis, the clone formatting, DNA synthesis, and western blotting for protein of PCNA and MAPK pathway were employed. RESULTS: beta-ionone inhibited the cell proliferation, cellular mitosis, clone formatting and DNA synthesis and reduced expression of PCNA protein in MDA-MB 435 cells. The inhibitory frequency (IF) showed a dose-dependent responses as the concentrations of beta-ionone increased. Seven days after treatment with various concentrations of beta-ionone, as mentioned above, the inhibition rates were 45.65%, 71.24%, 81.53%, and 84.93%, respectively. Its IC50 value was 42.0 micromol/L for MDA-MB 435 cells. The IF from cellular mitosis of MDA-MB 435 cells treated by beta-ionone were - 34.57%-58.857% at 24 h and - 30.05%-75.12% at 48 h, from the clone formatting assay, - 4.44%-63.79% at 24 h and 6.42%-95.55% at 48 h, from DNA synthesis, 17.00%-57.56% at 24h and 62.25%-78.35% at 48 h. The further study was found that beta-ionone inhibited the expression of PCNA which to be related to cell cycle and reduced ERK, MEK-1 proteins expression and promoted the expression of JNK and MKP-1 proteins related to MAPK pathway in MDA-MB 435 cells. CONCLUSION: beta-ionone could inhibit MDA-MB 435 cells proliferation by regulating MAPKs pathway. It may be one of the effects of beta-ionone in anticancer.
OBJECTIVE: To investigate the effect of cell proliferation in humanbreast cancer cells (MDA-MB 435), which has non-receptor of estrogen (Er), induced by beta-ionone. MDA-MB 435 cells were treated with different beta-ionone concentrations (25, 50, 100 and 200 micromol/L), with a negative control. METHODS: Such as curve of cell growth, cellular mitosis, the clone formatting, DNA synthesis, and western blotting for protein of PCNA and MAPK pathway were employed. RESULTS:beta-ionone inhibited the cell proliferation, cellular mitosis, clone formatting and DNA synthesis and reduced expression of PCNA protein in MDA-MB 435 cells. The inhibitory frequency (IF) showed a dose-dependent responses as the concentrations of beta-ionone increased. Seven days after treatment with various concentrations of beta-ionone, as mentioned above, the inhibition rates were 45.65%, 71.24%, 81.53%, and 84.93%, respectively. Its IC50 value was 42.0 micromol/L for MDA-MB 435 cells. The IF from cellular mitosis of MDA-MB 435 cells treated by beta-ionone were - 34.57%-58.857% at 24 h and - 30.05%-75.12% at 48 h, from the clone formatting assay, - 4.44%-63.79% at 24 h and 6.42%-95.55% at 48 h, from DNA synthesis, 17.00%-57.56% at 24h and 62.25%-78.35% at 48 h. The further study was found that beta-ionone inhibited the expression of PCNA which to be related to cell cycle and reduced ERK, MEK-1 proteins expression and promoted the expression of JNK and MKP-1 proteins related to MAPK pathway in MDA-MB 435 cells. CONCLUSION:beta-ionone could inhibit MDA-MB 435 cells proliferation by regulating MAPKs pathway. It may be one of the effects of beta-ionone in anticancer.