The Contrary Effects of Sirt1 on MCF7 Cells Depend on CD36 Expression Level

Abstract

BackgroundBreast cancer is one of the most aggressive and pervasive cancers identified in females. Sirt1 and CD36 both exert an essential role toward the oncogenic signaling in breast cancer cells. As reported, the adrenergic signaling could promote the malignancy of breast cancer. This study focuses specifically on the role of Sirt1/CD36 in the proliferation of MCF-7 breast cancer cells and also investigates their response to the α2-adrenergic agonist dexmedetomidine (Dex). Materials and MethodsExpression of Sirt1 and CD36 was measured in breast cancer tissue by immunohistochemistry. We cultured MCF7 cells and treated cells with resveratrol (RSV) or Dex. Western blot analysis was performed to quantify the protein expression levels. The methyl thiazolyl tetrazolium (MTT) assay was applied to detect cell proliferation. ResultsCompared with normal adjacent tissues, Sirt1 increased and CD36 decreased in cancer tissues. RSV, a Sirt1 activator, increased the proliferation of MCF-7 cells at low concentration but exerted cytotoxicity effect at higher concentration. Sirt1 activation increased the expression of CD36 at higher concentration. Dex treatment gradually increased the proliferation of MCF7 cells in a dose-dependent manner and downregulated the expression of Sirt1/CD36. Interestingly, overexpression of Sirt1 via RSV pretreatment could suppress Dex-stimulated proliferation of breast cancer, accompanied with CD36 upregulation. Conclusionsthough expression of Sirt1 increased in breast cancer progression, overexpression of Sirt1 could inhibit MCF7 proliferation, which may be associated with CD36 upregulation. In addition, the promotion effect of Dex on MCF7 cells, which may be associated with the Sirt1/CD36 inhibition, could be weakened by Sirt1 activation via RSV.