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Since then, studies have shown that the overexpression of PKC drives tumor development via synergistic activation of several cell-survival and mitotic pathways, including nuclear factor-κB (NF-κB), signal transducer and activator of transcription 3 (Stat3), phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt), and extracellular signal-regulated kinase (ERK) [151,152]
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