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A network pharmacology-based approach to explore the molecular mechanism of Aidi injection against prostate cancer
Sheng Guo1,2,3, Qiuping Zhang1,2, Xiaolan Li1
1Key Laboratory of Longevity and Aging-related Diseases of Chinese Ministry of Education & Center for Translational Medicine, Guangxi Key Laboratory of Bioactive Molecules Research and Evaluation & College of Pharmacy, Guangxi Medical University, 22 Shuangyong Road, Nanning, 530021, China.
Objective:
To explore the molecular mechanism of Aidi injection in the treatment of prostate cancer (PCa).
Materials And Methods:
CCK-8 and colony formation assays were used to detect the effects of Aidi on PC3 and DU145 cells; effects on the cell cycle and apoptosis of DU145 cells were detected by flow cytometry; effects on migration and invasion of PC3 and DU145 cells were detected by wound healing and transwell assay, respectively. The main active components of Aidi, their corresponding targets, and PCa associated pathways were predicted and analyzed by network pharmacology. Then predicted key targets and related signaling pathways were further verified by western blotting. The potential active components of Aidi were predicted by molecular docking technology.
Results:
Aidi significantly inhibited the proliferation, colony formation, migration, and invasion of PC3 and DU145 cells; Aidi induced apoptosis and cell cycle G2/M phase arrest of DU145 cells. Network pharmacology analysis yielded 36 potential core targets of Aidi against PCa, and the top 10 signaling pathways including MAPK, PI3K-Akt, and HIF-1α and so on were enriched. Western blotting confirmed that Aidi upregulated the expression levels of p-JNK, p-p38, p-ERK, and ERK in DU145 cells. Molecular docking study showed that kaempferol, (Z)-1-(2,4-dihydroxyphenyl)-3-(4-hydroxyphenyl)prop-2-en-1-one, 7-O-methylisomucronulatol, calycosin, and N-salicylidene-salicylamine can be well binding with JNK and p38.
Conclusion:
Aidi could inhibit PCa cell proliferation and metastasis through induction of apoptosis and cell cycle arrest, which may be related to activating JNK and p38 signaling pathway.
Insights
Aidi injection effectively inhibits prostate cancer (PCa) cell proliferation and metastasis by inducing apoptosis and cell cycle arrest. This mechanism involves the activation of the JNK and p38 signaling pathways.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Prostate cancer (PCa) remains a significant global health challenge.
- Understanding the molecular mechanisms of traditional therapies like Aidi injection is crucial for improving treatment outcomes.
Purpose of the Study:
- To elucidate the molecular mechanisms by which Aidi injection exerts its anti-prostate cancer effects.
- To identify key molecular targets and pathways involved in Aidi's action against PCa cells.
Main Methods:
- Cell viability, proliferation, apoptosis, cell cycle, migration, and invasion assays were performed on PCa cell lines (PC3 and DU145).
- Network pharmacology and molecular docking were employed to predict active components, targets, and pathways.
- Western blotting was used to validate key target protein expression.
Main Results:
- Aidi significantly inhibited PCa cell proliferation, colony formation, migration, and invasion.
- Aidi induced apoptosis and G2/M phase cell cycle arrest in DU145 cells.
- Network pharmacology identified 36 core targets and pathways including MAPK, PI3K-Akt, and HIF-1α; Western blotting confirmed upregulation of p-JNK, p38, p-ERK, and ERK.
Conclusions:
- Aidi injection demonstrates potent anti-prostate cancer activity by inhibiting cell proliferation and metastasis.
- The observed effects are mediated through the induction of apoptosis and cell cycle arrest, potentially via the JNK and p38 signaling pathways.
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