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The miR-145-5p/CD36 pathway mediates PCB2-induced apoptosis in MCF-7 cells
Yuan Yuan,Caihua Xue,Qiang Wu,Mengjie Wang,Jiahua Liu,Longfei Zhang,Qianwen Xing,Jingyan Liang,Hua Wu,Zhi Chen 한국유전학회 2021 Genes & Genomics Vol.43 No.2
Background Procyanidin B2 (PCB2) can increase the levels of anti-infammatory and immune mediators. Objectives However, its molecular mechanism in human breast cancer remains unclear. This study aimed to investigate the antitumor efect of PCB2 on MCF-7 cells and to examine the underlying mechanism. Methods The fow cytometry and EdU incorporation assays were measured the PCB2-induced BMECs. The expression levels of infammatory factors and immune response genes were upregulated in MCF-7 cells, high-throughput sequencing was used to detect diferentially expressed genes in blank and PCB2-treated MCF-7 cells. Results The results showed that PCB2 induced the apoptosis of MCF-7 cells. CD36 profles were afected in MCF-7 cells. Additionally, prediction software identifed 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 diferentially expressed miRNA miR145-5p 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 efect of PCB2 on CD36 expression by binding CD36 and subsequently regulating apoptosis, the immune response and anti-infammatory pathways. These results provide theoretical and experimental support for the treatment of breast cancer.
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