Biochemical and Biophysical Research Communications
Regular ArticleEstradiol Increases IRS-1 Gene Expression and Insulin Signaling in Breast Cancer Cells
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TAZ enhances mammary cell proliferation in 3D culture through transcriptional regulation of IRS1
2018, Cellular SignallingDifferent molecular signaling sustaining adiponectin action in breast cancer
2016, Current Opinion in PharmacologyCitation Excerpt :Higher circulating levels of leptin and TNF, found in obese women, enhance breast tumor growth as supported by in vitro and in vivo studies [5]. In addition, it is worth mentioning that the increased estrogen biosynthesis by adipose tissue, possibly in conjunction with elevated levels of insulin, insulin-like growth factor, contribute to mammary tumorigenesis [6]. On the other hand, an inverse correlation is reported between obesity and adiponectin, for which low levels of adiponectin constitute a risk factor for mammary cancer [7].
Effects of 17β-estradiol on cardiac Na<sup>+</sup>/K<sup>+</sup>-ATPase in high fat diet fed rats
2015, Molecular and Cellular EndocrinologyCross-talk between estradiol receptor and EGFR/IGF-IR signaling pathways in estrogen-responsive breast cancers: Focus on the role and impact of proteoglycans
2014, Matrix BiologyCitation Excerpt :Mounting evidence suggests that the cross-talk between non-genomic ERα action and growth factor receptor pathways is one mechanism in the development of endocrine-resistance (Nicholson and Johnston, 2005). Treatment of breast cancer cells with estrogens triggers IGF-I signaling through up-regulation of several components of this pathway such as IGF-IR, IRS-1 and IGF-I (Mauro et al., 2001). These upregulated proteins act locally in autocrine loops to mediate the biologic effects of estrogen.
Resveratrol regulates the cell viability promoted by 17β-estradiol or bisphenol A via down-regulation of the cross-talk between estrogen receptor α and insulin growth factor-1 receptor in BG-1 ovarian cancer cells
2013, Food and Chemical ToxicologyCitation Excerpt :Several studies have reported that the IGF-1R pathway triggered by IGF-1 is also regulated by a non-genomic pathway of E2 and the interaction between E2 and IGF-1 signaling pathways plays an important role in growth of estrogen sensitive cancer cells (Hamelers and Steenbergh, 2003; Massarweh and Schiff, 2006). In this case, IRS-1, a direct target protein of IGF-1R, exerts a key role in mediating the cross-talk between ERα and IGF-1R and linking IGF-1R to downstream signaling pathways like the PI3-kinase and the ERK pathways (Mauro et al., 2001; Molloy et al., 2000; Surmacz et al., 1998). In particular, phosphorylation of IRS-1 successively induces phosphorylation of Akt via PI3-kinase and, finally, up-regulation of proliferative signaling proteins in the cell cycle, such as cyclin D1 (Dufourny et al., 1997).
Indole-3-Carbinol disrupts Estrogen Receptor-alpha dependent expression of Insulin-like Growth Factor-1 Receptor and Insulin Receptor Substrate-1 and proliferation of human breast cancer cells
2012, Molecular and Cellular EndocrinologyCitation Excerpt :Knock down of IRS-1 can also reduce the IGF-1-dependent transcriptional activity of unliganded ERα (Sisci et al., 2007). In mice, ERα induces IRS1 transcription (Mauro et al., 2001), and E2 has been shown to stimulate IGF1R transcript levels (Stewart et al., 1990). Together with our previous report (Marconett et al., 2010), our results have defined the cellular cascade by which I3C disrupts the proliferation of ERα expressing human breast cancer cells through the loss of IGF1 signaling.
- 1
L.M. and M.S. contributed equally to this study.
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To whom correspondence and reprint requests should be addressed at Dipartimento di Biologia Cellulare, Università degli Studi della Calabria, 87030 Arcavacata-Rende Cosenza, Italy. Fax: (39) (0984) 492911. E-mail: [email protected].