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

Chuanming Lin,

Shuiling Xie, M. Wang

et al.

BMC Cancer, Journal Year: 2025, Volume and Issue: 25(1)

Published: April 30, 2025

Diffuse large B-cell lymphoma (DLBCL) is an aggressive and DLBCL cells are highly sensitive to ferroptosis. The purpose of this research was evaluate the role molecular mechanism peroxiredoxin 1 (PRDX1) on ferroptosis in DLBCL. expression PRDX1 tissues detected using bioinformatics analysis reverse transcription quantitative PCR. impacts cell proliferation, apoptosis, migration, invasion, were assessed through a series vitro experiments. A xenograft tumor model constructed verify roles vivo. Transcriptome sequencing conducted identify PRDX1-mediated signaling pathways. Anisomycin, agonist mitogen-activated protein kinase (MAPK), used explore modulation MAPK pathway. upregulated knockdown inhibited promoted suppressed growth. boosted erastin-induced by increasing levels iron MDA, while decreasing GSH. It also COX2 GPX4 SLC7A11 levels. reduced phosphorylation MEK ERK both under conditions with or without erastin induction. MAPK/ERK pathway anisomycin, significantly reversed inhibitory effects malignant behaviors promotion facilitates obstacles progression inhibiting pathway, offering potential treatment strategy for treatment.

Language: Английский

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

Chuanming Lin,

Shuiling Xie, M. Wang

et al.

BMC Cancer, Journal Year: 2025, Volume and Issue: 25(1)

Published: April 30, 2025

Diffuse large B-cell lymphoma (DLBCL) is an aggressive and DLBCL cells are highly sensitive to ferroptosis. The purpose of this research was evaluate the role molecular mechanism peroxiredoxin 1 (PRDX1) on ferroptosis in DLBCL. expression PRDX1 tissues detected using bioinformatics analysis reverse transcription quantitative PCR. impacts cell proliferation, apoptosis, migration, invasion, were assessed through a series vitro experiments. A xenograft tumor model constructed verify roles vivo. Transcriptome sequencing conducted identify PRDX1-mediated signaling pathways. Anisomycin, agonist mitogen-activated protein kinase (MAPK), used explore modulation MAPK pathway. upregulated knockdown inhibited promoted suppressed growth. boosted erastin-induced by increasing levels iron MDA, while decreasing GSH. It also COX2 GPX4 SLC7A11 levels. reduced phosphorylation MEK ERK both under conditions with or without erastin induction. MAPK/ERK pathway anisomycin, significantly reversed inhibitory effects malignant behaviors promotion facilitates obstacles progression inhibiting pathway, offering potential treatment strategy for treatment.

Language: Английский

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