Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2015
[Nongenomic effects of estrogen on extracellular signal-regulated kinases through initiating transient calcium flux in endometrial cancer].
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Zhang Li-li, Wang Jian-liu
Аннотация
OBJECTIVE: To study the mechanism on extracellular signal-regulate kinases (ERK) signal transduction by calcium influx initiated by combination of estrogen with calcium channels or estrogen receptor in endometrial cancer cell Ishikawa.
METHODS: Confocal test was used to determine the relative calcium mobilization by stimulation of estrodiol together with and without the inhibition of ICI182780 and nifedipine. Western-blotting was used to detect the protein expression of phosphorylated ERK1/2 (P-ERK1/2) in the same condition.
RESULTS: The transient calcium flux initiated by 17β-estrodiol (E2) and a membrane-impermeable conjugate of estrogen and bovine serum albumin (E2-BSA), and the calcium mobilization could be inhibited by ICI182780 and nifedipine in 1 min. In Ishikawa cells, phosphorylation of ERK1/2 was stimulated by E2, and the phosphorylation could not be inhibited by E2 after the combination with ICI182780 in 5 min and in 30 min. The phosphorylation also could not be inhibited by E2-BSA after the combination with nifedipine in 5 min, but in 30 min the phosphorylation was decreased. The phosphorylation of ERK by E2-BSA was decreased by the combination with nifedipine in 30 min.
CONCLUSION: The transient calcium flux initiated by estrogen has an effect on the activation of ERK signal pathway in endometrial carcinoma cells.
METHODS: Confocal test was used to determine the relative calcium mobilization by stimulation of estrodiol together with and without the inhibition of ICI182780 and nifedipine. Western-blotting was used to detect the protein expression of phosphorylated ERK1/2 (P-ERK1/2) in the same condition.
RESULTS: The transient calcium flux initiated by 17β-estrodiol (E2) and a membrane-impermeable conjugate of estrogen and bovine serum albumin (E2-BSA), and the calcium mobilization could be inhibited by ICI182780 and nifedipine in 1 min. In Ishikawa cells, phosphorylation of ERK1/2 was stimulated by E2, and the phosphorylation could not be inhibited by E2 after the combination with ICI182780 in 5 min and in 30 min. The phosphorylation also could not be inhibited by E2-BSA after the combination with nifedipine in 5 min, but in 30 min the phosphorylation was decreased. The phosphorylation of ERK by E2-BSA was decreased by the combination with nifedipine in 30 min.
CONCLUSION: The transient calcium flux initiated by estrogen has an effect on the activation of ERK signal pathway in endometrial carcinoma cells.