Oncology Medical News about estrogen receptor positive or negative breast cancer;Leptin-signaling

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Leptin-signaling inhibition results in efficient anti-tumor activity in estrogen receptor positive or negative breast cancer
Breast Cancer Research, 06/18/09

Gonzalez RR et al. - In a study in which pegylated leptin peptide receptor antagonist 2 (PEG-LPrA2) was used to evaluate whether inhibition of leptin signaling has differential impact on the expression of pro-angiogenic and pro-proliferative molecules and growth of human estrogen receptor positive (ER+) and negative (ER-) BC xenografts hosted by immunodeficient mice, it was shown that leptin signaling plays an important role in growth of both ER+ and ER- 4T1-breast cancer (BC) that is associated with leptin regulation of pro-angiogenic and pro-proliferative molecules. These data provide support for the potential use of leptin-signaling inhibition as a novel treatment of ER+ and ER- BC.

Methods

To test the contribution of leptin signaling to BC growth and expression of leptin-targeted molecules, PEG-LPrA2 treatment was applied to severe immunodeficient mice hosting established ER+ (MCF-7 cells; ovariectomized/supplemented with E2) and ER- BC xenografts (MDA-MB231 cells).
To further assess leptin and PEG-LPrA2 effects on ER+ and ER- BC, the expression of VEGF and VEGFR2 (protein and mRNA) were investigated in cell cultures.

Results

PEG-LPrA2 more effectively reduced the growth of ER+ (>40 fold) than ER- BC (2 fold) and expression of pro-angiogenic (VEGF/VEGFR2, leptin/leptin receptor OB-R, and interleukin 1 receptor type I, IL-1R tI) and pro-proliferative molecules (proliferating cell nuclear antigen, PCNA and cyclin D1) in ER+ than in ER- BC.
Mouse tumor stroma in ER+ BC expressed high levels of VEGF and leptin that was induced by leptin signaling.
Leptin up-regulated the transcriptional expression of VEGF/VEGFR2 in MCF-7 and MDA-MB231 cells.

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