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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Antioxidants, Breast Neoplasms, Cell Line, Tumor, Cell Proliferation, Dose-Response Relationship, Drug, Enzyme-Linked Immunosorbent Assay, Female, Humans, Janus Kinases, Leptin, Phosphorylation, STAT3 Transcription Factor, Signal Transduction, Stilbenes, Transcriptional Activation.
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Are the antiproliferative effects of pterostilbene on breast cancer in vitro via inhibition of constitutive and leptin-induced Janus kinase/signal transducer and activator of transcription activation? Context: The hormone leptin is implicated in breast carcinogenesis in obese women. One mechanism is through its activation of Janus kinase/signal transducer and activator of transcription (JAK/STAT3) and apoptosis dysregulation. We have shown that the antioxidant pterostilbene inhibits proliferation and induces apoptosis in breast cancer. Therefore, the goal of this study was to evaluate the effect of pterostilbene on cell proliferation and JAK/STAT3 signaling in leptin-stimulated breast cancer. Breast cancer cells were treated with leptin alone or in combination with pterostilbene. Detection of cell proliferation and JAK/STAT3 signaling were performed using enzyme-linked immunosorbent assay protocols. Statistical analysis was performed with analysis of variance and Tukey post hoc analysis. Pterostilbene suppresses constitutive as well as leptin-induced JAK/STAT3 activation. Pterostilbene treatment also inhibited leptin-induced cell proliferation.
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Pterostilbene has an inhibitory effect on leptin-stimulated breast cancer in vitro through reduction of cell proliferation and JAK/STAT3 signaling, a critical regulatory component of tumorigenesis in obesity-related breast cancer. Final Decision: yes