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Oridonin attenuated human PC-3 cell activity by modulating the Wnt/β-catenin signaling
Shuling Zhang1, Annamalai Vijayalakshmi2, Lingjun Meng3
1Department of Pharmacy, Tongchuan Hospital of Traditional Chinese Medicine, China.
Background:
Prostate cancer (PC) prevention is effectively achieved through its inhibition. Oridonin (ORD), an active diterpenoid isolated from Rabdosia rubescens, has been shown to have an inhibitory effect on PC cells, although its impact on PC is unknown.
Objectives:
The present work investigated the actions and probable mechanisms of ORD on cellular proliferation, apoptosis, PC, and the wingless-type MMTV integration site family member 2 (Wnt)/β-catenin signaling pathway using the androgen-independent PC-3 cell line.
Material And Methods:
In this study, cell viability was analyzed with MTT assay method, apoptotic morphology determined using DAPI dye method, while protein (CD1333, OCT-4, Nanog, SOX-2 & Aldh1A1) and mRNA expressions were analyzed with western blotting and real time polymerase chain reaction (PCR).
Results:
We demonstrated a concentration-dependent ORD inhibition of PC-3 cell proliferation and inhibition of induction apoptosis. Furthermore, ORD decreased PC-3 Wnt-2, phosphorylated glycogen synthase kinase-3 (p-GSK3), and β-catenin protein levels and downregulated cyclin-D1 and c-myc messenger ribonucleic acid (mRNA).
Conclusions:
Oridonin inhibited proliferation and induced apoptosis in PC-3 cells, with the findings suggesting that it acted via the Wnt/β-catenin pathway to exert its effects. This study demonstrates that ORD may impact PC.
Insights
Oridonin (ORD) inhibits prostate cancer (PC) cell proliferation and induces apoptosis. This natural compound may impact PC by modulating the Wnt/β-catenin signaling pathway.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Prostate cancer (PC) prevention requires effective inhibition strategies.
- Oridonin (ORD), a diterpenoid from Rabdosia rubescens, exhibits potential anti-PC effects.
- The specific mechanisms of ORD on PC remain largely unknown.
Purpose of the Study:
- To investigate the effects of Oridonin (ORD) on prostate cancer (PC) cell proliferation and apoptosis.
- To elucidate the probable mechanisms of ORD action, focusing on the Wnt/β-catenin signaling pathway.
- To utilize the androgen-independent PC-3 cell line for these investigations.
Main Methods:
- Cell viability assessed using MTT assay.
- Apoptotic morphology evaluated with DAPI staining.
- Protein and mRNA expression analyzed via Western blotting and real-time PCR, respectively.
Main Results:
- Oridonin demonstrated a dose-dependent inhibition of PC-3 cell proliferation.
- Oridonin induced apoptosis in PC-3 cells.
- ORD treatment decreased Wnt-2, p-GSK3, and β-catenin protein levels, and downregulated cyclin-D1 and c-myc mRNA.
Conclusions:
- Oridonin effectively inhibits PC-3 cell proliferation and induces apoptosis.
- The findings suggest Oridonin exerts its effects through the Wnt/β-catenin signaling pathway.
- Oridonin shows potential as a therapeutic agent impacting prostate cancer.
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