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. Author manuscript; available in PMC: 2014 May 14.
Published in final edited form as: Curr Drug Targets. 2012 Nov 6.

Figure 1. Apigenin targets insulin-like growth factor (IGF) axis and intracellular signaling to induce growth inhibition and apoptosis in prostate cancer cells.

Figure 1

Most IGF-1 within the extracellular intravascular compartment is sequestered in a binary complex with IGFBP-3 or in a ternary complex with IGFBP-3 and an ALS. Proteases secreted by the prostate cancer cell cleave IGFBP-3, causing the release of IGF-1. Free IGF-1 can then bind IGF-1R, causing its autophosphorylation and activation. Mediated through the phosphorylation and activation of IRS-1 scaffold protein, two primary intracellular signaling pathways are then activated, the MAPK/ERK pathway and the PI3K/Akt pathway, leading to cell cycle progression, cell proliferation, and cell survival. Apigenin can modulate this process by increasing both circulating and intracellular levels of IGFBP-3; decreasing circulating levels of IGF-1; inhibiting the secretion of proteases, such as PSA; inhibiting IGF-1R activation and downstream signaling; and inducing cell growth inhibition and apoptosis in prostate cancer cells.