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بیوشیمی مولکولی و سلولی 2013
جزئیات رویداد
اینستاگرام تی پی بین
همایش ، رویداد ، ژورنال
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  • simultaneous disruption of estrogen receptor and wnt/β-catenin signaling is involved in methyl amooranin-mediated chemoprevention of mammary gland carcinogenesis in rats

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    • تاریخ ارائه: 1392/07/24
    • تاریخ انتشار در تی پی بین: 1392/07/24
    • تعداد بازدید: 1020
    • تعداد پرسش و پاسخ ها: 0
    • شماره تماس دبیرخانه رویداد: -
     methyl-amoorain (methyl-25-hydroxy-3-oxoolean-12-en-28-oate, amr-me), a novel synthetic oleanane triterpenoid, exerts a striking chemopreventive effect against 7,12-dimethylbenz(a)anthracene (dmba)-induced rat mammary tumorigenesis through antiproliferative and proapoptotic actions. nevertheless, the underlying mechanisms of action remain to be established. as estrogen receptor (er) and canonical wnt/β-catenin signaling are involved in the development and progression of breast cancer, the current study was designed to investigate the effects of amr-me treatment on the expressions of er-α, er-β, β-catenin and cyclin d1 in rat mammary tumors induced by dmba. mammary tumor samples were harvested from an 18-week chemopreventive study in which amr-me (0.8–1.6 mg/kg) was shown to inhibit mammary carcinogenesis in a dose–response manner. the expressions of er-α, er-β, β-catenin, and cyclin d1 were determined by immunohistochemistry and reverse transcription-polymerase chain reaction. amr-me downregulated the expression of intratumor er-α and er-β and lowered the ratio of er-α to er-β. amr-me also reduced the expression, cytoplasmic accumulation, and nuclear translocation of β-catenin, the essential transcriptional cofactor for wnt signaling. furthermore, amr-me modulated the expression of cell growth regulatory gene cyclin d1, which is a downstream target for both er and wnt signaling. amr-me at 1.6 mg/kg for 18 weeks did not exhibit any hepatotoxicity or renotoxicity. the results of the present study coupled with our previous findings indicate that simultaneous disruption of er and wnt/β-catenin signaling possibly contributes to antiproliferative and apoptosis-inducing effects implicated in amr-me-mediated chemoprevention of dmba-induced breast tumorigenesis in rats. our results also suggest a possible cross-talk between two key regulatory pathways, namely er and wnt/β-catenin signaling, involved in mammary carcinogenesis and the value of simultaneously targeting these pathways to achieve breast cancer chemoprevention.

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