Synergistic anticancer therapy via ferroptosis using modified bovine serum albumin nanoparticles loaded with sorafenib and simvastatin

Kuche, Kaushik; Yadav, Vivek; Dharshini, M.; Ghadi, Rohan; Chaudhari, Dasharath; Date, Tushar; Jain, Sanyog

doi:10.1016/j.ijbiomac.2023.127254

Cited by 8 publications

(1 citation statement)

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“…Likewise, wogonin was shown to block Nrf2-induced resistance to ferroptosis [ 90 ]. Trigonelline, as another natural Nrf2 inhibitor, attenuates chemoresistance of PDAC cells [ 85 , 171 ] and has been also shown to efficiently suppress Nrf2-induced ferroptosis resistance in head-neck, breast, and lung cancer cells [ 85 , 168 , 169 , 170 , 171 , 172 , 173 , 174 ]. Digoxin and brucein-D were shown to inhibit Nrf2-dependent gemcitabine resistance of PDAC cells [ 173 , 175 ].…”

Section: Nrf2 Inhibitorsmentioning

confidence: 99%

The Role of Nrf2 in the Regulation of Mitochondrial Function and Ferroptosis in Pancreatic Cancer

Baiskhanova,

Schäfer

2024

Antioxidants

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The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) represents the master regulator of the cellular antioxidant response and plays a critical role in tumorigenesis. This includes a preventive effect of Nrf2 on cell death through ferroptosis, which represents an essential mechanism of therapy resistance in malignant tumors, such as pancreatic ductal adenocarcinoma (PDAC) as one of the most aggressive and still incurable tumors. Addressing this issue, we provide an overview on Nrf2 mediated antioxidant response with particular emphasis on its effect on mitochondria as the organelle responsible for the execution of ferroptosis. We further outline how deregulated Nrf2 adds to the progression and therapy resistance of PDAC, especially with respect to the role of ferroptosis in anti-cancer drug mediated cell killing and how this is impaired by Nrf2 as an essential mechanism of drug resistance. Our review further discusses recent approaches for Nrf2 inhibition by natural and synthetic compounds to overcome drug resistance based on enhanced ferroptosis. Finally, we provide an outlook on therapeutic strategies based on Nrf2 inhibition combined with ferroptosis inducing drugs.

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