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National Journal of Andrology ; (12): 828-837, 2017.
Article in Chinese | WPRIM | ID: wpr-812870

ABSTRACT

Objective@#To explore the apoptosis-inducing effect of the Chinese medicinal compound CFF-1 on prostate cancer cells and its related molecular mechanisms.@*METHODS@#Normal prostate WPMY-1 cells and prostate cancer LNCaP, CWR22Rv1, PC3 and DU145 cells were treated in dehydrated alcohol with CFF-1 at 0, 2, 5, or 10 mg/ml for 24 hours. Then the viability of the prostate cells was detected by morphological observation, MTT and CCK-8 assay, nuclear condensation and disruption measured by DAPI staining, the cell cycle and apoptosis calculated by flow cytometry, the activity of the PI3K/AKT/FOXO1 signaling pathway and the expressions of its downstream apoptosis- and cycle-related proteins determined by Western blot.@*RESULTS@#CFF-1 significantly arrested the cell cycle in the G1 phase, decreased the cell viability and increased the nuclear condensation and disruption in a dose-dependent manner, and elevated the apoptosis rate of prostate cancer cells. At the molecular level, CFF-1 dose-dependently reduced the activity of the PI3K/AKT signaling pathway and phosphorylation of the FOXO1 protein, increased the transcription activity of FOXO1, and eventually regulated the expressions of cell apoptosis- and cycle-related genes.@*CONCLUSIONS@#The Chinese medicinal compound CFF-1 can significantly inhibit the growth, arrest the cycle, and induce the apoptosis of prostate cancer cells by decreasing the activity of the PI3K/AKT/FOXO1 signaling pathway, which suggests its potential clinical application value in the treatment of prostate cancer.


Subject(s)
Humans , Male , Antineoplastic Agents, Phytogenic , Pharmacology , Apoptosis , Cell Cycle , Cell Division , Cell Line, Tumor , Cell Proliferation , Cell Survival , Drugs, Chinese Herbal , Pharmacology , Forkhead Box Protein O1 , Metabolism , Neoplasm Proteins , Metabolism , Phosphatidylinositol 3-Kinases , Metabolism , Phosphorylation , Prostatic Neoplasms , Drug Therapy , Metabolism , Pathology , Proto-Oncogene Proteins c-akt , Metabolism , Signal Transduction
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