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<p>Osteosarcoma (OS) presents significant treatment challenges due to chemoresistance. This study explores the molecular mechanisms underlying chemoresistance in OS, focusing on the novel fusion gene RPS27-RPS24. Using single-cell multi-omics techniques, we identified a significant upregulation of RPS27-RPS24 in chemoresistant OS cells. Our analyses revealed that RPS27-RPS24 enhances glutaminase (GLS)-mediated glutamine metabolism and inhibits copper-induced cell death, thereby promoting chemoresistance. In vitro experiments with adriamycin-resistant (ADMR) OS cells confirmed that overexpression of RPS27-RPS24 leads to increased cell viability and proliferation under chemotherapy. In vivo studies further validated these findings, demonstrating that targeting glutamine metabolism can reverse chemoresistance. Our results suggest that the RPS27-RPS24 fusion gene plays a critical role in OS chemoresistance through metabolic reprogramming, providing a potential therapeutic target for improving OS treatment outcomes.</p><p></p>

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Single-cell multi-omics elucidates the role of RPS27-RPS24 fusion gene in osteosarcoma chemoresistance and metabolic regulation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月25日

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  • Zhiwei Tao,
  • Pingan Zou,
  • Zhengxu Yang,
  • Tao Xiong,
  • Zhi Deng,
  • Qincan Chen

摘要

Osteosarcoma (OS) presents significant treatment challenges due to chemoresistance. This study explores the molecular mechanisms underlying chemoresistance in OS, focusing on the novel fusion gene RPS27-RPS24. Using single-cell multi-omics techniques, we identified a significant upregulation of RPS27-RPS24 in chemoresistant OS cells. Our analyses revealed that RPS27-RPS24 enhances glutaminase (GLS)-mediated glutamine metabolism and inhibits copper-induced cell death, thereby promoting chemoresistance. In vitro experiments with adriamycin-resistant (ADMR) OS cells confirmed that overexpression of RPS27-RPS24 leads to increased cell viability and proliferation under chemotherapy. In vivo studies further validated these findings, demonstrating that targeting glutamine metabolism can reverse chemoresistance. Our results suggest that the RPS27-RPS24 fusion gene plays a critical role in OS chemoresistance through metabolic reprogramming, providing a potential therapeutic target for improving OS treatment outcomes.