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The antiproliferative effects of pterostilbene on breast cancer in vitro are via inhibition of constitutive and leptin-induced Janus kinase/signal transducer and activator of transcription activation. Am J Surg 2011 Nov;202(5):541-4

Date

09/29/2011

Pubmed ID

21944294

DOI

10.1016/j.amjsurg.2011.06.020

Scopus ID

2-s2.0-80055021226 (requires institutional sign-in at Scopus site)   37 Citations

Abstract

BACKGROUND: 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.

METHODS: 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.

RESULTS: Pterostilbene suppresses constitutive as well as leptin-induced JAK/STAT3 activation. Pterostilbene treatment also inhibited leptin-induced cell proliferation.

CONCLUSIONS: 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.

Author List

McCormack D, Schneider J, McDonald D, McFadden D

Author

John G. Schneider MD Assistant Professor in the Surgery department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

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