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<p>Tumor angiogenesis facilitates cancer progression by supporting tumor growth and metastasis. MicroRNA-155 (miR-155) plays a pivotal role in regulating angiogenesis through both direct effects on tumor and endothelial cells and indirect modulation via exosomal communication. This review highlights miR-155’s pro-angiogenic influence on endothelial cell behavior and tumor microenvironment remodeling. Additionally, exosomal miR-155 enhances intercellular communication, promoting vascularization in several cancers. Emerging therapeutic strategies include miR-155 inhibition using antagomirs, exosome-mediated delivery systems, and modulation of pathways such as JAK2/STAT3 and TGF-β/SMAD2. Targeting miR-155 represents a promising approach to hinder tumor angiogenesis and improve cancer therapy outcomes.</p>

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Dual role of miR-155 and exosomal miR-155 in tumor angiogenesis: implications for cancer progression and therapy

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年5月19日

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  • Qusay Mohammed Hussain,
  • Ali Fawzi Al-Hussainy,
  • Gaurav Sanghvi,
  • R. Roopashree,
  • Aditya Kashyap,
  • D. Alex Anand,
  • Rajashree Panigrahi,
  • Nargiz Shavazi,
  • Sada Ghalib Taher,
  • Mariem Alwan,
  • Mahmood Jawad,
  • Hiba Mushtaq

摘要

Tumor angiogenesis facilitates cancer progression by supporting tumor growth and metastasis. MicroRNA-155 (miR-155) plays a pivotal role in regulating angiogenesis through both direct effects on tumor and endothelial cells and indirect modulation via exosomal communication. This review highlights miR-155’s pro-angiogenic influence on endothelial cell behavior and tumor microenvironment remodeling. Additionally, exosomal miR-155 enhances intercellular communication, promoting vascularization in several cancers. Emerging therapeutic strategies include miR-155 inhibition using antagomirs, exosome-mediated delivery systems, and modulation of pathways such as JAK2/STAT3 and TGF-β/SMAD2. Targeting miR-155 represents a promising approach to hinder tumor angiogenesis and improve cancer therapy outcomes.