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Published on: January 26, 2019
The miR-145-5p/CD36 pathway mediates PCB2-induced apoptosis in MCF-7 cells
Yuan Yuan1,2, Caihua Xue3, Qiang Wu3
1School of Nursing, Yangzhou University, Yangzhou, 225009, People's Republic of China.
Background:
Procyanidin B2 (PCB2) can increase the levels of anti-inflammatory and immune mediators.
Objectives:
However, its molecular mechanism in human breast cancer remains unclear. This study aimed to investigate the antitumor effect of PCB2 on MCF-7 cells and to examine the underlying mechanism.
Methods:
The flow cytometry and EdU incorporation assays were measured the PCB2-induced BMECs. The expression levels of inflammatory factors and immune response genes were upregulated in MCF-7 cells, high-throughput sequencing was used to detect differentially expressed genes in blank and PCB2-treated MCF-7 cells.
Results:
The results showed that PCB2 induced the apoptosis of MCF-7 cells. CD36 profiles were affected in MCF-7 cells. Additionally, prediction software identified a miR-145-5p binding site in the CD36 sequence. Luciferase reporter assays and Western blot analysis were used to verify the regulatory relationships between the differentially expressed miRNA miR-145-5p and CD36. MiR-145-5p and its key target (CD36) constitute a potential miRNA-mRNA regulatory pair. Functional studies in MCF-7 cells revealed that CD36 promotes but miR-145-5p inhibits apoptosis.
Conclusion:
Overall, these data suggest that miR-145-5p inhibits the enhancing effect of PCB2 on CD36 expression by binding CD36 and subsequently regulating apoptosis, the immune response and anti-inflammatory pathways. These results provide theoretical and experimental support for the treatment of breast cancer.
Insights
Procyanidin B2 (PCB2) induces breast cancer cell apoptosis. It regulates miR-145-5p and CD36, impacting immune and anti-inflammatory pathways for potential breast cancer treatment.
Area of Science:
- Molecular Biology
- Cancer Research
- Immunology
Background:
- Procyanidin B2 (PCB2) is known to modulate anti-inflammatory and immune responses.
- The precise molecular mechanisms of PCB2 in human breast cancer are not fully understood.
Purpose of the Study:
- To investigate the antitumor effects of PCB2 on MCF-7 human breast cancer cells.
- To elucidate the underlying molecular mechanisms, including gene and miRNA expression.
- To explore the role of PCB2 in regulating apoptosis, immune response, and inflammation.
Main Methods:
- Utilized flow cytometry and EdU incorporation assays to assess cell apoptosis and proliferation.
- Employed high-throughput sequencing to identify differentially expressed genes in response to PCB2.
- Verified miRNA-mRNA interactions using luciferase reporter assays and Western blot analysis.
Main Results:
- PCB2 treatment induced apoptosis in MCF-7 cells.
- Identified a regulatory relationship between miR-145-5p and its target CD36.
- Demonstrated that CD36 promotes apoptosis, while miR-145-5p inhibits it.
Conclusions:
- MiR-145-5p inhibits PCB2's enhancement of CD36 expression, thereby regulating apoptosis and inflammatory pathways.
- These findings suggest a novel mechanism for PCB2's action in breast cancer.
- Provide a theoretical and experimental basis for developing PCB2-based breast cancer therapies.
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