PRDX1 knockdown promotes erastin-induced ferroptosis and impedes diffuse large B-cell lymphoma development by inhibiting the MAPK/ERK pathway
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View abstract on PubMed
Summary
This summary is machine-generated.Knocking down peroxiredoxin 1 (PRDX1) enhances ferroptosis in diffuse large B-cell lymphoma (DLBCL) cells by inhibiting the MAPK/ERK pathway. This finding suggests PRDX1 as a potential therapeutic target for DLBCL treatment.
Area Of Science
- Oncology
- Cell Biology
- Molecular Mechanisms
Background
- Diffuse large B-cell lymphoma (DLBCL) is an aggressive hematological malignancy.
- DLBCL cells exhibit sensitivity to ferroptosis, a regulated form of cell death.
- Peroxiredoxin 1 (PRDX1) is implicated in cellular processes relevant to cancer progression.
Purpose Of The Study
- To investigate the role of PRDX1 in ferroptosis within DLBCL.
- To elucidate the molecular mechanisms by which PRDX1 influences ferroptosis and DLBCL progression.
Main Methods
- PRDX1 expression analysis in DLBCL tissues and cells via bioinformatics and qPCR.
- In vitro assessment of PRDX1's impact on DLBCL cell proliferation, apoptosis, migration, invasion, and ferroptosis.
- In vivo validation using a xenograft tumor model.
- Transcriptome sequencing to identify PRDX1-mediated pathways and MAPK/ERK pathway modulation using anisomycin.
Main Results
- PRDX1 expression is upregulated in DLBCL.
- PRDX1 knockdown inhibits DLBCL cell proliferation, migration, invasion, and tumor growth, while promoting apoptosis.
- PRDX1 knockdown enhances erastin-induced ferroptosis, indicated by increased iron and MDA, and decreased GSH, COX2, GPX4, and SLC7A11 protein levels.
- PRDX1 knockdown reduces MAPK/ERK pathway phosphorylation, an effect reversed by anisomycin.
Conclusions
- PRDX1 knockdown promotes ferroptosis and hinders DLBCL progression by inhibiting the MAPK/ERK pathway.
- Targeting PRDX1 represents a potential therapeutic strategy for DLBCL.
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