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자료유형
학술저널
저자정보
Yuan Yuan (Yangzhou University) Caihua Xue (Qinghai University) Qiang Wu (Qinghai University) Mengjie Wang (Qinghai University) Jiahua Liu (Qinghai University) Longfei Zhang (Qinghai University) Qianwen Xing (Qinghai University) Jingyan Liang (Yangzhou University) Hua Wu (Qinghai University) Zhi Chen (Yangzhou University)
저널정보
한국유전학회 Genes & Genomics Genes & Genomics Vol.43 No.2
발행연도
2021.1
수록면
161 - 171 (11page)

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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.

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