Up-regulating of RASD1 and apoptosis of DU-145 human prostate cancer cells induced by formononetin in vitro

Prostate cancer is one of the most prevalent malignant cancers in men. The isoflavone formononetin is a main active component of red clover plants. In the present study, we assessed the effect of formononetin on human prostate cancer DU-145 cells in vitro, and elucidated possible mechanisms. DU-145...

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Published inAsian Pacific journal of cancer prevention : APJCP Vol. 15; no. 6; pp. 2835 - 2839
Main Authors Liu, Xiao-Jia, Li, Yun-Qian, Chen, Qiu-Yue, Xiao, Sheng-Jun, Zeng, Si-En
Format Journal Article
LanguageEnglish
Published Thailand 01.01.2014
Subjects
Apoptosis - drug effects
bcl-2-Associated X Protein - metabolism
Blotting, Western
Cell Proliferation - drug effects
Flow Cytometry
Humans
In Vitro Techniques
Isoflavones - pharmacology
Male
Phytoestrogens - pharmacology
Prostatic Neoplasms - drug therapy
Prostatic Neoplasms - metabolism
Prostatic Neoplasms - pathology
Proto-Oncogene Proteins c-bcl-2 - metabolism
ras Proteins - metabolism
Tumor Cells, Cultured
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Summary:Prostate cancer is one of the most prevalent malignant cancers in men. The isoflavone formononetin is a main active component of red clover plants. In the present study, we assessed the effect of formononetin on human prostate cancer DU-145 cells in vitro, and elucidated possible mechanisms. DU-145 cells were treated with different concentrations of formononetin and cell proliferation was assessed by MTT assay, cell apoptosis by Hoechst 33258 and flow cytometry, and protein levels of RASD1, Bcl-2 and Bax by Western blotting. The results showed that formononetin inhibited the proliferation of DU-145 cells in a dose-dependent manner. DU-145 cells treated with different concentrations of formononetin displayed obvious morphological changes of apoptosis under fluorescence microscopy. In addition, formononetin increased the proportion of early apoptotic DU-145 cells, down-regulated the protein levels of Bcl-2 and up-regulated those of RASD1 and Bax. The level of RASD1 reached its maximum at 48 h post-treatment, and rapidly decreased thereafter. Together, we present evidence that formononetin triggered cell apoptosis through the mitochondrial apoptotic pathway by up-regulating RASD1.
ISSN:1513-7368
2476-762X
DOI:10.7314/APJCP.2014.15.6.2835