Yuan Yuan1,2, Caihua Xue3, Qiang Wu3, Mengjie Wang3, Jiahua Liu3, Longfei Zhang3, Qianwen Xing3, Jingyan Liang4, Hua Wu5, Zhi Chen6. 1. School of Nursing, Yangzhou University, Yangzhou, 225009, People's Republic of China. 2. Nagano College of Nursing, Komagane, 3994117, Japan. 3. College of Agriculture and Animal Husbandry, Qinghai University, No.251 Ningda Road, Xining, 810016, Qinghai, People's Republic of China. 4. School of Medicine, Yangzhou University, Yangzhou, 225009, People's Republic of China. 5. College of Agriculture and Animal Husbandry, Qinghai University, No.251 Ningda Road, Xining, 810016, Qinghai, People's Republic of China. qhwuhua@163.com. 6. College of Animal Science and Technology, Yangzhou University, Yangzhou, 225009, People's Republic of China. zhichen@yzu.edu.cn.
Abstract
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.
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.