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PRMT4 Reduced Erastin-Induced Ferroptosis in Nasopharyngeal Carcinoma Cisplatin-Resistant Cells by Nrf2/GPX4 Pathway
Xiaoping Pu1, Hong Wu2, Xiaoyan Liu2
1Wuxi Xishan People's Hospital.
Abstract:
Nasopharyngeal carcinoma (NPC) is one of the common malignant tumors in clinic. In the current study, we aim to investigate the effects of PRMT4 on erastin-induced ferroptosis in NPC by cisplatin resistant. PRMT4 expression in patients with NPC by cisplatin was upregulated. PRMT4 upregulation promoted cell growth of erastin-induced ferroptosis in NPC cisplatin-resistant cells. PRMT4 downregulation reduced cell growth of erastin-induced ferroptosis in NPC cisplatin-resistant cells. PRMT4 promoted tumor volume in mice model of erastin-induced NPC by cisplatin. PRMT4 upregulation reduced erastin-induced ferroptosis in NPC cisplatin-resistant cells by mitochondrial damage. PRMT4 upregulation induced Nrf2 protein expression in model of erastin-induced NPC by cisplatin. Nrf2 reduced the effects of si-PRMT4 on cell growth of erastin-induced ferroptosis in NPC cisplatin-resistant cells. Nrf2 inhibitor reduced the effects of PRMT4 on cell growth of erastin-induced ferroptosis in NPC cisplatin-resistant cells. Nrf2 reduced the effects of si-PRMT4 on erastin-induced ferroptosis in NPC cisplatin-resistant cells by mitochondrial damage. PRMT4 protein interlinked with Nrf2 protein to decrease Nrf2 ubiquitination. Methylation increased PRMT4 DNA stability. Collectively, our data reveal that PRMT4 reduced erastin-induced ferroptosis in NPC cisplatin-resistant cells by Nrf2/GPX4 pathway, suggesting that targeting PRMT4 may present as a potential strategy against the development of NPC.
Insights
Protein arginine methyltransferase 4 (PRMT4) promotes nasopharyngeal carcinoma (NPC) growth by inhibiting ferroptosis. Targeting PRMT4 may offer a new strategy against cisplatin-resistant NPC.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Nasopharyngeal carcinoma (NPC) is a common malignancy.
- Cisplatin resistance is a significant challenge in NPC treatment.
- Ferroptosis, a regulated form of cell death, is implicated in cancer therapy.
Purpose of the Study:
- To investigate the role of PRMT4 in erastin-induced ferroptosis in cisplatin-resistant NPC.
- To elucidate the molecular mechanisms underlying PRMT4's function in NPC.
Main Methods:
- Analysis of PRMT4 expression in NPC patients.
- Cellular assays to assess cell growth and ferroptosis.
- In vivo studies using a mouse model.
- Western blot analysis to detect protein expression and interaction.
Main Results:
- PRMT4 expression was upregulated in cisplatin-resistant NPC.
- PRMT4 overexpression promoted NPC cell growth and tumor volume.
- PRMT4 inhibited erastin-induced ferroptosis by reducing mitochondrial damage.
- PRMT4 interacted with Nrf2, increasing its expression and stability, thereby reducing Nrf2 ubiquitination.
Conclusions:
- PRMT4 reduces erastin-induced ferroptosis in cisplatin-resistant NPC via the Nrf2/GPX4 pathway.
- PRMT4 upregulation contributes to NPC progression and chemoresistance.
- Targeting PRMT4 could be a potential therapeutic strategy for NPC.
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