Abstract
Obesity is a risk factor of breast cancers. As leptin, a hormone mainly secreted by white adipocytes, elicits proliferative effects in some cell types, we tested the hypothesis that leptin could influence human breast cancer MCF-7 cell growth. Here we show that MCF-7 cells express leptin receptors and respond to human recombinant leptin by STAT3 and p42/p44 MAPkinase activations and by increased proliferation. These findings suggest that leptin could act in vivo as a paracrine/endocrine growth factor towards mammary epithelial cells thus contributing to explain why obesity is a risk factor of developing breast cancers.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acute-Phase Proteins / metabolism
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Adipocytes / cytology
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Adipocytes / drug effects
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Adipocytes / physiology*
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Breast Neoplasms / pathology*
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Cell Division / drug effects*
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DNA, Neoplasm / biosynthesis
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DNA-Binding Proteins / metabolism
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Female
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Humans
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Leptin / pharmacology*
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Mitogen-Activated Protein Kinase 1 / metabolism
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Mitogen-Activated Protein Kinase 3
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Mitogen-Activated Protein Kinases / metabolism
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Obesity / complications
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Recombinant Proteins / pharmacology
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Reverse Transcriptase Polymerase Chain Reaction
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Risk Factors
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STAT3 Transcription Factor
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Thymidine / metabolism
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Trans-Activators / metabolism
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Tumor Cells, Cultured
Substances
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Acute-Phase Proteins
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DNA, Neoplasm
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DNA-Binding Proteins
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Leptin
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Recombinant Proteins
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STAT3 Transcription Factor
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STAT3 protein, human
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Trans-Activators
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Mitogen-Activated Protein Kinase 1
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Mitogen-Activated Protein Kinase 3
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Mitogen-Activated Protein Kinases
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Thymidine