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In another study, IGF-1 was shown to regulate glucose metabolism in cancer cells with the involvement of kallikrein-related peptidase 10 (KLK10) and the knockdown of KLK10 markedly inhibited glucose metabolism and PI3K/Akt/mTOR signaling activation, a process that could be reversed by IGF-1, suggesting that IGF-1 and KLK10 serve as potential targets for regulating metabolic remodeling in colon cancer (79)

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Pyo and colleagues showed that GHK-Cu at concentrations as low as 1 μM promoted dermal papilla cell proliferation and beta-catenin signaling in mouse models