SENP1 knockdown potentiates the apoptosis, cell cycle arrest, and reduces cisplatin resistance of diffuse large B...

Area of Science:

• Oncology
• Cell Biology
• Biochemistry

Background:

• Diffuse large B cell lymphoma (DLBCL) is a significant hematologic malignancy.
• Ferroptosis, a regulated form of cell death, plays a role in DLBCL pathogenesis.
• Sentrin-specific protease 1 (SENP1) is implicated as an oncogene in various cancers.

Purpose of the Study:

• To investigate the role of SENP1 in DLBCL progression.
• To explore the potential mechanism of SENP1 involving ferroptosis in DLBCL.
• To assess SENP1's impact on chemoresistance in DLBCL.

Main Methods:

• Gene expression analysis (GEPIA, RT-qPCR) and protein analysis (Western blot) for SENP1.
• Cell viability assays (CCK-8) and flow cytometry for apoptosis and cell cycle.
• Biochemical assays (TBARS, BODIPY probe, iron level assessment) to measure ferroptosis.
• Assessment of cisplatin resistance using CCK-8 and flow cytometry.

Main Results:

• SENP1 expression is upregulated in DLBCL tissues and cells.
• SENP1 knockdown decreased cell viability, induced apoptosis and cell cycle arrest, and enhanced cisplatin sensitivity.
• SENP1 depletion promoted ferroptosis in both parental and cisplatin-resistant DLBCL cells.
• The ferroptosis inhibitor Fer-1 reversed the effects of SENP1 inhibition.

Conclusions:

• SENP1 promotes DLBCL progression and cisplatin resistance.
• SENP1 inhibition induces ferroptosis, thereby hindering DLBCL development and chemoresistance.
• Targeting SENP1 may represent a novel therapeutic approach for DLBCL.