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. Author manuscript; available in PMC: 2019 May 1.
Published in final edited form as: Mol Cancer Res. 2018 Feb 16;16(5):869–879. doi: 10.1158/1541-7786.MCR-17-0508

Figure 6.

Figure 6

Proposed model illustrating leptin-mediated upregulation in CSC/EMT-related genes and phenotype. Our findings suggest that obesity in MMTV-Wnt-1 mice promotes both an excess of leptin production in the tumor microenvironment (normal mammary tissue) and an upregulation in tumor expression of the leptin receptor and CSC/EMT-related genes. They also indicate that leptin signaling promotes a CSC/EMT-related phenotype, including increased CSC enrichment and cell viability, migration, and invasion, and specifically regulates the expression of Foxc2, Twist2, Vim, Akt3, and Sox2 in triple-negative mammary tumor cells. We hypothesize that these genes may mediate the observed leptin-induced CSC/EMT-related phenotype and that leptin regulates these genes via stimulation of the JAK2/STAT3 and/or PI3K/Akt pathways. Black arrows indicate effects observed in this study, solid blue arrows indicate pathways known from the literature, and dotted blue arrows indicate hypothesized mechanisms.