ArticleGenes & genomics2021
The miR-145-5p/CD36 pathway mediates PCB2-induced apoptosis in MCF-7 cells.
Article in Genes & genomics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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10 authors at 3 institutions in 2 countries.
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Abstract
backgroundProcyanidin B2 (PCB2) can increase the levels of anti-inflammatory and immune mediators.
objectivesHowever, 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.
methodsThe 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.
resultsThe 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.
conclusionOverall, 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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