The crosstalk between cholesterol synthesis pathway and TGF-beta in pancreatic cancer

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Although statins led better survival outcomes, the anti-proliferative effects inColorectal cancer (CRC) cells differ in statins (simvastatin >=fluvastatin > atorvastatin> pravastatin). Indeed, the recurrence rate of CRC patients with pravastatin had nodifference compared to patients without statin. As the underlying mechanism, statinsexcept pravastatin showed the anti-cancer effects by inhibiting EZH2-mediated genesilencing of p27KIP1. As a novel epigenetic anti-cancer strategy, a simvastatin plusclassII HDAC inhibitor synergistically induced the anti-proliferative effects byinhibiting EZH2-modulated HDAC5 induction. Thus, as a novel mechanism of statin-inducedanti-cancer effects, EZH2-mediated epigenetic mechanism was identified. Although statinmay lead to survival benefits in CRC patients, its anti-cancer effects differ in statins,suggesting that the kind of statins should be considered in clinical settings.