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Updated: Apr 18, 2026
Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
Published on: June 20, 2015
[Experimental study on anti-pancreatic cancer effect of oridonin]
Hui Wang1, Yuan-Fang Wang, Tian-Gui Liu
1Guangdong Province Key Laboratory of Biotechnology Drug Candidate, Guangdong Pharmaceutical University, China.
Objective:
To investigate the apoptotic effect of oridonin in human pancreatic cancer cells PANC-1, and to explore the underlying mechanism.
Methods:
MTT assay was used to measure the cell viability. Apoptosis was determined by confocal laser scanning microscope after Hoechst 33342 staining and flow cytometry analysis after PI staining. The regulation of JNK and p38 MAPK signaling pathway proteins was examined by Western blot analysis.
Results:
Treatment with oridonin for 24 h resulted in a marked decrease in cell viability in a dose-dependent manner. The IC50 value was determined as 49.80 μmol/L for 24 h. After treatment with 50 micromol/L and 80 μmol/L oridonin for 24 h, typical apoptotic nucleus alterations were observed with confocal laser scanning microscope and apoptotic rates of PANC-1 cells increased by flow cytometry analysis. Treatment with 80 μmol/L oridonin down-regulated protein expression of JNK, p38 and increased the expression of p-JNK, p-p38. Furthermore, 80 μmol/L oridonin treatment decreased the expression of down-stream proteins Caspase-9, Caspase-3 and PARP in the apoptotic pathway as well as activated the cleavage of Caspase-9.
Conclusion:
Oridonin can induce apoptosis of PANC-1 cells through JNK and p38 MAPK pathway proteins.
Insights
Oridonin induces apoptosis in human pancreatic cancer cells (PANC-1) by down-regulating JNK and p38 MAPK pathways. This natural compound shows potential for pancreatic cancer treatment, warranting further investigation.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Pancreatic cancer remains a significant global health challenge with limited effective treatments.
- Identifying novel therapeutic agents that induce cancer cell apoptosis is crucial.
Purpose of the Study:
- To investigate the apoptotic effects of oridonin on human pancreatic cancer cells (PANC-1).
- To elucidate the underlying molecular mechanisms, focusing on the JNK and p38 MAPK signaling pathways.
Main Methods:
- Cell viability was assessed using MTT assays.
- Apoptosis was quantified via confocal microscopy (Hoechst 33342 staining) and flow cytometry (PI staining).
- Western blotting analyzed the expression of key proteins in the JNK and p38 MAPK pathways.
Main Results:
- Oridonin significantly reduced PANC-1 cell viability in a dose-dependent manner (IC50 = 49.80 μmol/L at 24h).
- Oridonin treatment induced characteristic apoptotic morphological changes and increased apoptotic rates in PANC-1 cells.
- Oridonin modulated JNK and p38 MAPK signaling, down-regulating total protein levels while increasing phosphorylation, and affected downstream apoptosis-related proteins (Caspase-9, Caspase-3, PARP).
Conclusions:
- Oridonin effectively induces apoptosis in PANC-1 human pancreatic cancer cells.
- The mechanism involves the modulation of the JNK and p38 MAPK signaling pathways.
- Oridonin presents a potential therapeutic candidate for pancreatic cancer treatment.
