RTA-408 exerts antitumour and radiosensitizing effects via activation of the JNK pathway and inhibits GBM progression. These findings highlight its potential as a novel therapeutic strategy for the treatment of GBM.
Western blot analysis revealed that RTA-408 modulated apoptosis-related protein expression and inhibited reactive oxygen species production, thereby reducing oxidative stress in TMZ-resistant glioblastoma cells. These findings indicate that RTA-408 is not only a promising alternative for TMZ-sensitive glioblastoma but also a first-line treatment option for TMZ-resistant glioblastoma.
5 months ago
Journal
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KEAP1 (Kelch Like ECH Associated Protein 1) • CASP3 (Caspase 3)
Additionally, we explore the complementary role of NRF1, an ER-resident transcription factor that cooperates with NRF2 to maintain proteostasis and mediate stress resilience. Finally, we examine the therapeutic landscape of NRF2-targeted agents including ML385, PRL295, Omaveloxolone, and DHTI, highlighting their potential for therapeutic use tailored to tumor stage and cellular context.
We selected A549/DDP cells as a research model and demonstrated through a series of experimental manipulations that RTA-408 inhibited the growth of A549/DDP cells and inhibited the ubiquitinated degradation of nuclear receptor coactivator 4 through down-regulation of WW structural domain-containing E3 ubiquitin-protein ligase 1 (WWP1), which further induced the development of ferritinophagy and ferroptosis. We report for the first time that RTA-408 overcomes cisplatin-resistant lung cancer by targeting WWP1-mediated ferritinophagy and ferroptosis.