Leptin and cancer: from cancer stem cells to metastasis

    1. Philipp E Scherer1,2,3
    1. 1Department of Internal Medicine, Touchstone Diabetes Center
      2Department of Cell Biology
      3Simmons Cancer Center, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-8549, USA
    1. (Correspondence should be addressed to P E Scherer at Department of Internal Medicine, Touchstone Diabetes Center, University of Texas Southwestern Medical Center; Email: philipp.scherer{at}utsouthwestern.edu)

    Abstract

    There is growing evidence that obesity is a risk factor of cancer incidence and mortality. Hence, the identification of the mechanistic links between obesity and cancer progression is emerging as a topic of widespread interest. Recently, several groups have addressed the functional roles of leptin, an adipocyte-derived adipokine, for mammary tumor progression. In this issue of Endocrine-Related Cancer, Zheng et al. study the role of leptin on tumor growth in a xenograft model of MMTV-Wnt1-derived cancer cells. They study growth of these cancer cells in the context of obese animals, such as ob/ob mice (lacking leptin) and db/db mice (lacking functional leptin receptors (LEPR)) and find that leptin triggers LEPR-positive cancer stem cell differentiation, thereby promoting tumor cell survival. These findings highlight the therapeutic potential for leptin and leptin signaling in the context of mammary tumor growth.

    • Revision received 6 June 2011
    • Accepted 16 June 2011
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