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. 2020 Aug 31;12(9):2661. doi: 10.3390/nu12092661

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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The molecular mechanism of action of OOS in several preclinical models has been described and involves regulation of cell proliferation by blockage of S phase and G2-M transition. OOS also induces caspase-dependent cell death which leads to PARP cleavage. As a consequence of the apoptotic process, DNA damage occurs and this is readout by increases in pHistone H2AX. OOS also inhibits stemness and self-renewal as indicated by the down-regulation of several stem-cell markers. Finally, an important action of OOS is related to the modulation of the immune system, as indicated by changes in the production of several cytokines. IL6: interleukin-6; IL10: interleukin 10; IFNα: interferon alpha; TNFα: tumor necrosis factor alpha; IL1β: interleukin-1 beta; Cox2: cyclo-oxygenase-2; IL12: interleukin 12; IFNγ: interferon gamma; CD133: cluster of differentiation 133; CD44: cluster of differentiation 44; SOX2: sex determining region Y-box 2; RB: retinoblastoma protein; PARP: Poly-ADP Ribose Polymerase.