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Targeting RPLP2 Triggers DLBCL Ferroptosis by Decreasing FXN Expression
Jiaxing Guo1,2, Bokang Yan3, Lingshu Li1
1Department of Hematology, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, Zhuzhou 412007, China.
Biomedicines
|June 26, 2025
Summary
Ribosomal Protein Lateral Stalk Subunit P2 (RPLP2) drives diffuse large B-cell lymphoma (DLBCL) progression by inhibiting ferroptosis. Targeting RPLP2 with Destruxin b offers a novel therapeutic strategy for DLBCL treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Ribosomal Protein Lateral Stalk Subunit P2 (RPLP2) is implicated in cancer development.
- The role of RPLP2 in diffuse large B-cell lymphoma (DLBCL) is not well understood.
Purpose of the Study:
- To investigate the role of RPLP2 in DLBCL progression.
- To explore RPLP2's impact on ferroptosis and identify potential therapeutic targets.
Main Methods:
- siRNA-mediated knockdown of RPLP2 in DLBCL cells.
- RT-qPCR, immunohistochemistry, CCK8, colony formation, and transwell assays.
- Lipid ROS, iron assays, and xenograft mouse models were used to assess ferroptosis and in vivo efficacy.
Main Results:
- Elevated RPLP2 expression correlates with poor prognosis in DLBCL patients.
- RPLP2 knockdown inhibits DLBCL cell proliferation and migration.
- RPLP2 regulates ferroptosis by modulating ferroptosis suppressor frataxin (FXN) activity.
- Destruxin b targets RPLP2 to suppress DLBCL, with combination therapy showing enhanced anti-tumor effects.
Conclusions:
- RPLP2 acts as an oncogene in DLBCL.
- A novel regulatory axis involving RPLP2 and FXN-mediated ferroptosis is identified.
- RPLP2 is a potential therapeutic target for DLBCL treatment.
