Silencing Of Cluster Determinant 36 Transmitted By Gold Nanoparticles Inhibits The Occurrence And Progression Of Breast Cancer By Down-Regulating The Peroxisome Proliferative Activated Receptor Signaling Pathway

Breast cancer is the most commonly diagnosed tumor in women worldwide. Although a range of therapeutic strategies have been developed in recent years, the outcome for patients is often poor. The purpose of this study was to explore the molecular mechanisms of the membrane glycoprotein CD36 in breast cancer. Cells from breast cancer cell lines were transfected with gold nanoparticles protected by liposomes, as gene vectors. Cell counting kit 8 assays were performed to determine cell variability, EdU straining assays were used to evaluate cell proliferation, and colony formation assays were performed to detect cell colony ability. The number of cells involved in migration and invasion was counted using Transwell assays. Lymphangiogenesis formation was assessed using lymphangiogenesis formation assay. Xenograft tumor mice were established, to analyze the effects of CD36. Quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, and immunohistochemistry (IHC) were performed to estimate the expression of genes. Silencing of CD36 inhibited cell variability, proliferation, colony formation, lymphangiogenesis, and repressed cell migration and invasion in vitro. Overexpression of PPAR reversed the effects of the silencing of CD36, and the effects of PPAR upregulation were blocked by PPAR inhibitor. In vivo, tumor growth and lymphangiogenesis and PPAR activation were suppressed by the silencing of CD36. Silencing of CD36 also inhibited the variability, proliferation, colony formation, lymphangiogenesis, migration and invasion of breast cancer cells by suppressing PPAR signaling pathway activation. The CD36 gene was transfected with gold nanoparticles which improved the efficiency of gene transfection. The use of gold nanoparticles provides a new way to study the effects of genes on tumor cells.