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<p>Uveal melanoma (UM), a prevalent intraocular malignancy with a high rate of metastasis, particularly to the liver, presents a significant therapeutic challenge due to the absence of effective treatments. Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) are under scrutiny for their roles in cancer, with lncRNA-NEAT1 identified as a key contributor to tumor growth. Our study delves into the aberrant expression of NEAT1, miR-506-3p, and STAT3 in UM cells compared with retinal pigment epithelial cells, revealing their impact on UM cell proliferation, migration, and invasion. Interventions targeting NEAT1 inhibition or miR-506-3p overexpression restrict UM cell viability, migration, and invasion. Conversely, increasing NEAT1 expression or suppressing miR-506-3p enhances these biological behaviors. Bioinformatic tools and dual-luciferase assays validated the specific binding of miR-506-3p to <i>NEAT1</i> and its regulatory effect on <i>STAT3</i>. Rescue experiments further confirmed these interactions, contributing to a comprehensive understanding of the NEAT1/miR-506-3p/STAT3 axis in UM. The NEAT1/miR-506-3p/STAT3 axis has emerged as a promising diagnostic and therapeutic target for UM, providing a novel perspective on the pathogenesis of this challenging malignancy.</p> Graphical abstract <p></p>

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The NEAT1/miR-506-3p/STAT3 axis promotes uveal melanoma progression and represents a potential therapeutic target

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月11日

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  • Xiangyu Liu,
  • Mengdi Zhang,
  • Lijie Hao,
  • Xiaohan Ren,
  • Chunling Xu

摘要

Uveal melanoma (UM), a prevalent intraocular malignancy with a high rate of metastasis, particularly to the liver, presents a significant therapeutic challenge due to the absence of effective treatments. Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) are under scrutiny for their roles in cancer, with lncRNA-NEAT1 identified as a key contributor to tumor growth. Our study delves into the aberrant expression of NEAT1, miR-506-3p, and STAT3 in UM cells compared with retinal pigment epithelial cells, revealing their impact on UM cell proliferation, migration, and invasion. Interventions targeting NEAT1 inhibition or miR-506-3p overexpression restrict UM cell viability, migration, and invasion. Conversely, increasing NEAT1 expression or suppressing miR-506-3p enhances these biological behaviors. Bioinformatic tools and dual-luciferase assays validated the specific binding of miR-506-3p to NEAT1 and its regulatory effect on STAT3. Rescue experiments further confirmed these interactions, contributing to a comprehensive understanding of the NEAT1/miR-506-3p/STAT3 axis in UM. The NEAT1/miR-506-3p/STAT3 axis has emerged as a promising diagnostic and therapeutic target for UM, providing a novel perspective on the pathogenesis of this challenging malignancy.

Graphical abstract