Study on the autophagy of prostate cancer PC-3 cells induced by oridonin

Li-Hong Ye1, Wang-Jian Li, Xiao-Qiang Jiang

  • 1Department of Urology Surgery, Shaoxing County Central Hospital, Shaoxing 312030, China. ylh7966@126.com

Insights

Oridonin (ORI) inhibits prostate cancer cell growth by inducing autophagy. This process involves increased autophagosomes and key protein expression, suggesting ORI

Area of Science:

  • Cell Biology
  • Cancer Research
  • Pharmacology

Background:

  • Prostate cancer remains a significant health concern, necessitating novel therapeutic strategies.
  • Autophagy, a cellular degradation process, plays a complex role in cancer development and treatment.
  • Oridonin (ORI), a natural compound, has shown potential cytotoxic effects against cancer cells.

Purpose of the Study:

  • To elucidate the mechanism by which oridonin (ORI) induces autophagy in prostate cancer PC-3 cells.
  • To investigate the impact of ORI on cell proliferation, ultrastructure, and autophagy-related markers in PC-3 cells.

Main Methods:

  • Cell viability was assessed using the MTT assay.
  • Ultrastructural changes were observed via light microscopy, scanning electron microscopy (SEM), and transmission electron microscopy (TEM).
  • Autophagy was evaluated through acridine orange (AO) staining for acidic vesicular organelles (AVOs), Western blot for MAP1-LC3, and RT-PCR for beclin 1 mRNA.

Main Results:

  • ORI significantly inhibited PC-3 cell proliferation in a dose- and time-dependent manner.
  • SEM and TEM revealed cellular shrinkage, microvilli loss, chromatin condensation, and increased autophagosomes.
  • ORI treatment upregulated LC3 expression and beclin 1 mRNA levels, which were reversed by the autophagy inhibitor 3-methyladenine.

Conclusions:

  • Oridonin (ORI) effectively inhibits prostate cancer PC-3 cell growth.
  • ORI induces autophagy in PC-3 cells, characterized by morphological changes and altered expression of autophagy markers.
  • ORI demonstrates potential as an antitumor agent for prostate cancer through autophagy induction.