Fig. 1.

Crosstalk Signaling and miRNA Deregulation in Obesity Related Breast Cancer. Obesity induce hyperinsulinemia, overexpression of leptin, increasing estradiol due to aromatization, Insulin-like Growth Factor 1 (IGF-1) and also Vascular endothelial Growth Factor Receptor (VEGFR) expression. Activation of JAK-STAT pathway, RAS-RAF-MEK-MAPK pathway, PI3K-AKT pathway lead to activation of nuclear transcription that regulate gene expression necessary for suppressing autophagy, apoptosis, and increasing growth, proliferation, cell cycle progression, and cellular survival. Certain microRNAs (miRs) work to regulate expression of protein-coding genes needed in metabolic and carcinogenic process. Green arrow for up-regulation and red arrow for down-regulation. VEGF Vascular Endothelial Growth Factor, GPCR G protein coupled receptor, ER estrogen receptor, RAS Rat sarcoma, RAF serine threonine protein kinases protooncogene, MEK/MAP2K1 mitogen activated protein kinase kinase, ERK extracellular signal-regulated kinases, STAT signal tranducer and activator transcription, JAK2 Janus Kinase 2, IRS insulin receptor substrate, HIF-α Hypoxia Inducible Factor-α, CREB cAMP Response Element-Binding Protein, cAMP cyclic Adenosin Monophosphat, PI3K phosphoinositide inositol 3 kinases, AKT serine/threonine kinas, Mdm2 mouse double minute 2 homolog, BAD Bcl2 associated agonist cell death, GSK3 Glycogen Synthase Kinase 3, FOXO fork head box O, mTOR mechanistic target of Rapamycin Kinase, IκK I κKinase,. NFκB nuclear Factor κB