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. 2020 Aug 24;13:8463–8474. doi: 10.2147/OTT.S258680

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© 2020 Chen et al.

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Schema of the predicted mechanisms implicated in EC cells response to cisplatin and anti-miR-183. Suppression of miR-183 significantly increased the expression of FOXO1. Subsequently, FOXO1 promoted the expression of Bim and Noxa which were pro-apoptotic proteins. Under the apoptotic signaling caused by cisplatin, Bim and Noxa enhanced the dysfunction of mitochondria. As a result, mitochondria-derived apoptotic inducers such as cytochrome c and AIF were released from mitochondria into the cytosol of EC cells. Eventually, caspases-dependent apoptosis was triggered.