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Related Concept Videos

The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
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Related Experiment Video

Updated: Sep 18, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
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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
PubMed
Summary
This summary is machine-generated.

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.

Keywords:
DLBCLDestruxin bFXNRPLP2doxorubicinferroptosis

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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.