
doi: 10.3892/or.2018.6791
pmid: 30320364
Prostate cancer is a serious affliction worldwide. Although much progress has been made in the study of prostate cancer prevention and treatment, less attention has been paid to the molecular mechanism of the disease. The molecular arrangement by which Schisandrin B (Sch B) induces human prostate cancer cytotoxicity was comprehensively examined in the present study. As indicated by the results of flow cytometric and western blot analysis, Sch B could inhibit prostate cancer cell proliferation and promote DU145 and LNCaP cell apoptosis and S‑phase cell arrest. Moreover, real‑time PCR, flow cytometry and western blot result revealed that the cell apoptosis process induced by Sch B in LNCaP cells was associated with its capacity to generate oxidative stress, its inhibition of androgen receptor and the phosphorylation of PI3K/AKT and STA3/JAK2. The data from the present study demonstrated the antitumor effects and the potential pharmacological application of Sch B as an efficient drug for prostate cancer.
Male, STAT3 Transcription Factor, Prostatic Neoplasms, Apoptosis, Cell Cycle Checkpoints, Janus Kinase 2, Lignans, S Phase, Cyclooctanes, Oxidative Stress, Phosphatidylinositol 3-Kinases, Receptors, Androgen, Cell Line, Tumor, Humans, Polycyclic Compounds, Phosphorylation, Proto-Oncogene Proteins c-akt, Cell Proliferation, Signal Transduction
Male, STAT3 Transcription Factor, Prostatic Neoplasms, Apoptosis, Cell Cycle Checkpoints, Janus Kinase 2, Lignans, S Phase, Cyclooctanes, Oxidative Stress, Phosphatidylinositol 3-Kinases, Receptors, Androgen, Cell Line, Tumor, Humans, Polycyclic Compounds, Phosphorylation, Proto-Oncogene Proteins c-akt, Cell Proliferation, Signal Transduction
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