Leptin mediates a proliferative response in human MCF7 breast cancer cells

Dieudonné, Marie‐Noëlle; Machinal-Quélin, Florence; Serazin-Leroy, Valérie; Leneveu, Marie-Christine; Pecquery, René; Giudicelli, Yves

doi:10.1016/s0006-291x(02)00205-x

Cited by 259 publications

(243 citation statements)

References 30 publications

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“…Leptin and the leptin receptor have been characterized in MCF-7 breast cancer cell lines (32). Previous studies have demonstrated that immunodeficient mice hosting MCF-7 cells, which were treated with pegylated leptin peptide receptor antagonist 2 exhibited a significant reduction in the growth of tumor explants (33).…”

Section: Discussionmentioning

confidence: 99%

Leptin promotes the proliferation and migration of human breast cancer through the extracellular-signal regulated kinase pathway

Sun

2013

Molecular Medicine Reports

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Abstract. Obesity has been associated with an increased risk of postmenopausal breast cancer, which may be due to the expression of leptin. The aim of this study was to determine the role of leptin in the growth of breast cancer cells in nude mice, the proliferation and migration of MCF-7 human breast cancer cells and its downstream signaling pathway. The xenograft mouse model was elicited by injecting MCF-7 human breast cancer cells into the left back axilla and the tumor size was measured every other day. Leptin injected subcutaneously around the tumor site led to an increase in the size and weight of the tumor, whereas the leptin antagonist (LA) significantly inhibited the size and weight of the tumor. Leptin promoted the proliferation and migration of MCF-7 cells and LA inhibited it. The effects of leptin on increasing the size and weight of the tumor in the nude mice and the proliferation and migration of MCF-7 human breast cancer cells were eradicated by pretreatment with LA, the extracellular-signal regulated kinase (ERK) inhibitor PD98059. In the xenograft mouse model the leptin level was increased and leptin increased the phosphorylation of ERK in the MCF-7 cells, whereas LA significantly reduced the phosphorylation of ERK. These results indicated that leptin promotes the growth of breast cancer in the nude mice and increases the proliferation and migration of MCF-7 human breast cancer cells via the ERK pathway.

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Section: Discussionmentioning

confidence: 99%

Leptin promotes the proliferation and migration of human breast cancer through the extracellular-signal regulated kinase pathway

Sun

2013

Molecular Medicine Reports

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“…ever, new data suggest that leptin might be involved in mammary carcinogenesis (O'Brien et al, 1999;Dieudonne et al, 2002;Hu et al, 2002;Laud et al, 2002;Okumura et al, 2002;Cleary et al, 2003). Leptin and ObR have been found in normal and cancer mammary epithelium by immunohistochemistry with specific antibodies (Abs) (Ishikawa et al, 2004).…”

Section: Effects Of Leptin On Cancer Cells In Vitromentioning

confidence: 99%

Leptin and cancer

Garofalo

Surmacz

2005

Journal Cellular Physiology

543

497

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The prevalence of obesity has markedly increased over the past two decades, especially in the industrialized countries. While the impact of excess body weight on the development of cardiac disease and diabetes has been well documented, the link between obesity and carcinogenesis is just being recognized. This review will focus on the link between leptin, a cytokine that is elevated in obese individuals, and cancer development. First, we briefly discuss the biological functions of leptin and its signaling pathways. Then, we summarize the effects of leptin on different cancer types in experimental cellular and animal models. Next, we analyze epidemiological data on the relationship between obesity and the presence of cancer or cancer risk in patients. Finally, leptin as a target for cancer treatment and prevention will be discussed.

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“…Although several hundred adipokines have been discovered to date, several studies have focused on ADIPO and LEP as they are the most abundant, have been shown to directly affect the growth of several cancers including breast and are altered in opposing fashion with obesity (Dieudonne et al. 2002, 2006; Zhong et al. 2010).…”

Section: Discussionmentioning

confidence: 99%

“…Both are among the most abundant adipokines produced/secreted, are altered by obesity and have documented cell‐cycle regulatory effects on breast cancer cells (Dieudonne et al. 2002, 2006; Jarde et al. 2009).…”

Section: Introductionmentioning

confidence: 99%

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Voluntary physical activity counteracts the proliferative tumor growth microenvironment created by adipose tissue via high-fat diet feeding in female rats

Theriau

Connor

2017

Physiol Rep

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The adipokine secretion profile created from adipose tissue may represent the molecular mechanism behind the obesity‐breast cancer association. Two adipokines, adiponectin (ADIPO), and leptin (LEP), are altered with obesity and exert antagonistic effects on breast cancer proliferation. We set out to determine whether the adipose‐dependent tumor promoting growth environment created by a high‐fat diet (HFD) in female Sprague‐Dawley rats is altered compared to established responses in male rats and whether voluntary physical activity (PA) ameliorates any HFD‐dependent effects. We found that conditioned media (CM) created from the adipose tissue of female HFD‐fed rats increased the proliferation of MCF7 cells compared to those cells grown in CM prepared from lean adipose tissue. HFD‐CM inhibited AMPK and activated Akt signaling, decreased p27 phosphorylation at T198, reduced total p27 and AdiporR1 protein levels and promoted cell‐cycle entry. PA reversed the proliferative effects of HFD‐CM on MCF7 cells by preventing the effects of HFD on AMPK, Akt, p27 and AdipoR1, ultimately resulting in cell‐cycle withdrawal. Overexpressing AdipoR1 abolished the proliferative effects of the HFD‐CM on MCF7 cells and enhanced the anti‐proliferative effects PA on the HFD‐CM. Thus, PA represents a means to prevent deleterious obesity‐related alterations in tumor growth environment which are brought about by changes in adipokine secretion profile from adipose tissue in the presence of estrogen. Furthermore, although adipose produces hundreds of adipokines, the ADIPO:LEP ratio may serve to indicate the contribution of adipose in creating a tumor growth microenvironment.

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Leptin mediates a proliferative response in human MCF7 breast cancer cells

Cited by 259 publications

References 30 publications

Leptin promotes the proliferation and migration of human breast cancer through the extracellular-signal regulated kinase pathway

Leptin promotes the proliferation and migration of human breast cancer through the extracellular-signal regulated kinase pathway

Leptin and cancer

Voluntary physical activity counteracts the proliferative tumor growth microenvironment created by adipose tissue via high-fat diet feeding in female rats

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