Inhibitory effects of Schisandrin B on human prostate cancer cells

Oncol Rep. 2019 Jan;41(1):677-685. doi: 10.3892/or.2018.6791. Epub 2018 Oct 15.

Abstract

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.

MeSH terms

  • Apoptosis / drug effects
  • Cell Cycle Checkpoints / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cyclooctanes / pharmacology
  • Humans
  • Janus Kinase 2 / metabolism
  • Lignans / pharmacology*
  • Male
  • Oxidative Stress / drug effects
  • Phosphatidylinositol 3-Kinases / metabolism
  • Phosphorylation / drug effects
  • Polycyclic Compounds / pharmacology*
  • Prostatic Neoplasms / drug therapy*
  • Prostatic Neoplasms / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Receptors, Androgen / metabolism
  • S Phase / drug effects
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction / drug effects

Substances

  • Cyclooctanes
  • Lignans
  • Polycyclic Compounds
  • Receptors, Androgen
  • STAT3 Transcription Factor
  • schizandrin B
  • Phosphatidylinositol 3-Kinases
  • Janus Kinase 2
  • Proto-Oncogene Proteins c-akt