Figure 2.

Proposed mechanistic links between ghrelin axis and tumor growth and metastasis. Proposed model illustrating pathways through which the ghrelin axis exerts proliferative effects on cancer cells. UAG and AG have both been found to activate the PI3K/Akt pathway and stimulate cancer cell proliferation in low doses, though AG acts in a GHSR-1a dependent manner while UAG’s mechanism of activation is unknown. In1-ghrelin has been found to activate the MAPK/ERK pathway through an undiscovered mechanism. In1-ghrelin levels have also been found to correlate with GOAT levels, suggesting that acylation and corresponding activation of GHSR-1a may be possible, though In1-ghrelin has not been reported to alter Akt phosphorylation. GHSR-1b levels often parallel In1-ghrelin levels as well, and have been linked to increased tumor severity and metastasis.