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Article Abstract
Context: Cervical cancer (CC) ranks as one of the most common types of malignant tumors affecting women. CDDO-Me is derived from oleanolic acid, a pentacyclic triterpenoid obtained by chemical structural modification, which has been shown anti-tumor effects.
Results: CC cell proliferation was decreased by CDDO-Me both in vitro and in vivo. Mechanistically, CDDO-Me led to a reduction of intracellular mitochondrial volume and crista, or an increase of membrane density. The levels of ROS, Fe, MDA were increased while GSH was decreased. Meanwhile, the levels of protein expression of GPX4, Nrf2, NQO1 and FTH1 were observably inhibited by CDDO-Me. Specifically, ferroptosis triggered by CDDO-Me was reverted by DFO. It has been demonstrated that CDDO-Me-induced apoptosis and ferroptosis in CC cells is contingent upon the PI3K/AKT-mediated Nrf2/NQO1 pathway.
Conclusions: CDDO-Me induces CC cell lines apoptosis and ferroptosis through the PI3K/Nrf2 signaling pathway, for exerting anti-proliferation effects.
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| http://dx.doi.org/10.1016/j.fct.2025.115664 | DOI Listing |
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