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. Author manuscript; available in PMC: 2015 Jan 1.
Published in final edited form as: Best Pract Res Clin Endocrinol Metab. 2013 Nov 22;28(1):59–69. doi: 10.1016/j.beem.2013.11.005

Fig. 1.

Fig. 1

Model for APN-mediated suppression of cancer promoting pathways. In normal epithelial cells, APN is bound by T-cadherin and presented directly or indirectly to AdipoR1/R2 to inhibit signaling pathways activated in neoplasia. APN-activates AMPK, and inhibits PI3K/AKT, mTOR, MAPK and JAK/Stat pathways, or directly affects GSK3β to suppress cancer promoting pathways. Cancer cells down-regulate T-cadherin while AdipoR1/R2 expression persists and cancer promoting pathways prevail. One model is that ceramidase activity associated with AdipoR1/R2 weighs the balance in favor of cancer cell survival. T-cadherin expressed in the tumor vasculature promotes cancer as a pro-angiogenic factor in cooperation with APN (not shown [38,39]). Black arrows, activating pathways; red lines with bar: inhibitory pathways.