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Fig. 4 | BMC Cancer

Fig. 4

From: PRDX1 knockdown promotes erastin-induced ferroptosis and impedes diffuse large B-cell lymphoma development by inhibiting the MAPK/ERK pathway

Fig. 4

PRDX1 knockdown enhances erastin-induced ferroptosis in DLBCL cells through modulation of the MAPK/ERK pathway. A. Western blot analysis of p-ERK, total ERK, p-MEK, and total MEK protein expression in OCI-Ly3 and DB cells transfected with si-NC or si-PRDX1, and treated with DMSO, erastin, or MAPK/ERK pathway anisomycin treatment. B. Western blot analysis of p-ERK, total ERK, p-MEK, and total MEK protein expression in OCI-Ly3 and DB cells after PRDX1 knockdown only under DMSO treatment conditions. C. RT-qPCR analysis of PRDX1 expression in DLBCL cells treated with the MAPK/ERK pathway inhibitor (BVD-523). D. The viability of DLBCL cells following PRDX1 knockdown, erastin, DMSO, or anisomycin treatment was assessed using CCK-8 assay. E. The assessment of ferroptosis-related indicators, including MDA, iron, and GSH, was performed after the PRDX1 knockdown and treatment with erastin, DMSO, or anisomycin. F. Protein levels of COX2 and GPX4 were measured by western blot following PRDX1 knockdown, erastin, DMSO, or anisomycin treatment. **P < 0.01 vs. DMSO or si-NC (DMSO) group; ##P < 0.01 vs. si-NC (erastin) group; &P < 0.05, &&P < 0.01 vs. si-PRDX1 (erastin) group

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BMC Cancer

ISSN: 1471-2407

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