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<p>Cluster of Differentiation 47 (CD47) is regarded as a highly promising next-generation immunotherapy target following PD-1/PD-L1. It mediates tumor immune escape by transmitting a “don't eat me” signal through the signal regulatory protein alpha (SIRPα) pathway. However, the clinical application of existing antibody therapies remains constrained by erythrocyte toxicity, the antigen sink caused by widespread CD47 expression on normal cells, and recent setbacks in clinical trials. "Growing evidence establishes non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), as key upstream regulators of CD47. Here, we systematically review how these ncRNAs control CD47 gene expression, focusing on their impact on phagocytosis, drug resistance, and tumor microenvironment remodeling. Unlike antibody-mediated blockade, targeting the ncRNA–CD47 axis provides a unique avenue for genetic modulation, offering reduced systemic toxicity. We summarize these regulatory mechanisms and explore how exploiting these gene-regulatory networks can address the current challenges in CD47 immunotherapy.</p>

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Recent advances in the regulation of CD47 by non-coding RNAs and its therapeutic potential in cancer

  • 期刊论文

  • 发表日期：

    2026年5月7日

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  • Jingwen Hua,
  • Weijin Zhu,
  • Xiaochun Sun,
  • Huabiao Chen

摘要

Cluster of Differentiation 47 (CD47) is regarded as a highly promising next-generation immunotherapy target following PD-1/PD-L1. It mediates tumor immune escape by transmitting a “don't eat me” signal through the signal regulatory protein alpha (SIRPα) pathway. However, the clinical application of existing antibody therapies remains constrained by erythrocyte toxicity, the antigen sink caused by widespread CD47 expression on normal cells, and recent setbacks in clinical trials. "Growing evidence establishes non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), as key upstream regulators of CD47. Here, we systematically review how these ncRNAs control CD47 gene expression, focusing on their impact on phagocytosis, drug resistance, and tumor microenvironment remodeling. Unlike antibody-mediated blockade, targeting the ncRNA–CD47 axis provides a unique avenue for genetic modulation, offering reduced systemic toxicity. We summarize these regulatory mechanisms and explore how exploiting these gene-regulatory networks can address the current challenges in CD47 immunotherapy.