Figure 1.

Figure 1. From: The Role of Adiponectin in Cancer: A Review of Current Evidence.

Signaling pathways connecting adiponectin to carcinogenesis. Adiponectin may act on cancer tissues either by sequestrating growth factors at the prereceptor level or by binding to AdipoR1, AdipoR2, and T-cadherin. T-Cadherin has not been associated with downstream effector molecules and may serve as a coreceptor for adiponectin. Binding to AdipoR1 and AdipoR2, initiates a cascade of signaling molecules comprising, among others, activation of AMPK by the cofactors LKB1, APPL-1, and/or CaMKK; induction of Bax and cAMP/PKA; as well as inhibition of ERK1/2, PI3K/Akt, Wnt/β-catenin, nicotinamide adenine dinucleotide phosphate-oxidase/ROS/MAPK, NF-κB, Bcl-2, and JAK2/STAT3 signaling. Activated AMPK subsequently stimulates JNK, PP2A, and the cell cycle regulators p53/p21/p27, while negatively influencing fatty acid synthase (FAS)/ACC and the mTOR/S6K axis. Collectively, these effects result in reduced fatty acid and protein synthesis; decreased cellular growth, proliferation, and DNA-mutagenesis; and increased cell cycle arrest and apoptosis, thus negatively influencing carcinogenesis. Cross talk between the mentioned pathways adds further complexity to the adiponectin-induced signaling network. Finally, recent advances show that adiponectin can enhance ceramidase activity independently from AMPK via AdipoR1/R2, contributing to increased amounts of prosurvival S1P. The black and red lines indicate stimulatory and inhibitory effects, respectively. Trx, Thioredoxin.

Maria Dalamaga, et al. Endocr Rev. 2012 August;33(4):547-594.

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