Related Experiment Video
Updated: Jan 26, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Daucosterol induces autophagic-dependent apoptosis in prostate cancer via JNK activation
Ping Gao1,2, Xiaopeng Huang2, Tingting Liao3
1Department of Urology, Hospital of Chengdu University of Traditional Chinese Medicine.
Abstract:
Plant sterols (phytosterols) have been widely accepted as a natural anti-cancer agent in multiple malignant tumors. This study was designed to investigate the functions of daucosterol in prostate cancer progression and its possible molecular mechanisms. Our results showed that daucosterol inhibited cell proliferation and induced cell cycle arrest. Moreover, daucosterol treatment obviously promoted apoptosis and autophagy. An autophagy inhibitor, 3-methyladenine (3-MA) was proved to counteract daucosterol-triggered autophagy, growth inhibition, and apoptosis, indicating that daucosterol-induced apoptotic response was dependent on autophagy. Additionally, treatment with daucosterol resulted in increased phosphorylation of c-Jun N-terminal kinase (JNK). Furthermore, pre-treatment with a JNK-specific inhibitor SP600125 abated daucosterol-elicited autophagy and apoptotic cell death. Taken together, our findings demonstrated that daucosterol blocked prostate cancer growth at least partly through inducing autophagic-dependent apoptosis via activating JNK signaling, providing a promising candidate for the development of antitumor drugs in prostate cancer treatment.
Insights
Daucosterol, a plant sterol, inhibits prostate cancer growth by triggering programmed cell death (apoptosis) dependent on cellular recycling (autophagy) and activating the JNK signaling pathway.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Plant sterols, or phytosterols, are recognized for their anti-cancer properties.
- Prostate cancer remains a significant global health concern requiring novel therapeutic strategies.
Purpose of the Study:
- To investigate the anti-cancer effects of daucosterol on prostate cancer progression.
- To elucidate the molecular mechanisms underlying daucosterol's action in prostate cancer.
Main Methods:
- Cell proliferation assays and cell cycle analysis were performed.
- Apoptosis and autophagy were assessed using specific inhibitors and treatments.
- The involvement of c-Jun N-terminal kinase (JNK) signaling was examined using specific inhibitors.
Main Results:
- Daucosterol significantly inhibited prostate cancer cell proliferation and induced cell cycle arrest.
- Daucosterol promoted both apoptosis and autophagy, with autophagy being essential for the apoptotic response.
- Activation of JNK signaling was observed, and its inhibition blocked daucosterol-induced autophagy and apoptosis.
Conclusions:
- Daucosterol exhibits anti-prostate cancer activity by inducing autophagic-dependent apoptosis.
- The JNK signaling pathway plays a crucial role in mediating daucosterol's anti-cancer effects.
- Daucosterol represents a potential therapeutic candidate for prostate cancer treatment.
Related Concept Videos
Apoptosis
Autophagic Cell Death
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
Mechanisms of Retrovirus-induced Cancers
Frequency-dependent Selection
Temperature Dependence on Reaction Rate
Atoms, molecules, or ions must collide before they can react with each other. Atoms must be close together to form chemical bonds. This premise is the basis for a theory that explains many observations regarding chemical kinetics, including factors affecting reaction rates.
The collision theory is based on the postulates that (i) the reaction rate is proportional to the rate of reactant collisions, (ii) the reacting species collide in an orientation allowing contact between...
Drug Dependence

