Scholarlink

<p>Retinoblastoma (RB) is the most common primary intraocular malignancy in children, and its extraocular extension is closely linked to poor prognosis. However, the molecular drivers underlying local invasion remain incompletely defined. Here, we identify β‑1,4‑galactosyltransferase III (B4GALT3) as a glycosyltransferase selectively upregulated in highly proliferative MKI67⁺ RB subpopulations. B4GALT3 promotes RB cell proliferation, fibronectin adhesion, and invasion by enhancing β1-integrin glycosylation, thereby activating FAK signaling and inducing MMP2 expression to disrupt retinal epithelial barriers. Genetic modulation of B4GALT3 significantly altered both tumor burden and invasive behavior in orthotopic xenograft models. Structure-based virtual screening identified myricoside as a B4GALT3 inhibitor, which suppressed RB malignancy in vitro and in vivo. Overall, our findings uncover a B4GALT3–integrin–FAK axis as a key regulator of RB progression and highlight B4GALT3 inhibition as a promising therapeutic strategy for advanced RB.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

β1,4-galactosyltransferase III drives retinoblastoma invasion via activation of integrin-FAK axis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月23日

查看全文
  • Junjie Tang,
  • Jinmiao Li,
  • Meng Wang,
  • Yaoming Liu,
  • Hetian Sun,
  • Zhihui Zhang,
  • Yang Gao,
  • Chao Cheng,
  • Shuxia Chen,
  • Ping Zhang,
  • Siming Ai,
  • Shicai Su,
  • Youjin Hu,
  • Rong Lu

摘要

Retinoblastoma (RB) is the most common primary intraocular malignancy in children, and its extraocular extension is closely linked to poor prognosis. However, the molecular drivers underlying local invasion remain incompletely defined. Here, we identify β‑1,4‑galactosyltransferase III (B4GALT3) as a glycosyltransferase selectively upregulated in highly proliferative MKI67⁺ RB subpopulations. B4GALT3 promotes RB cell proliferation, fibronectin adhesion, and invasion by enhancing β1-integrin glycosylation, thereby activating FAK signaling and inducing MMP2 expression to disrupt retinal epithelial barriers. Genetic modulation of B4GALT3 significantly altered both tumor burden and invasive behavior in orthotopic xenograft models. Structure-based virtual screening identified myricoside as a B4GALT3 inhibitor, which suppressed RB malignancy in vitro and in vivo. Overall, our findings uncover a B4GALT3–integrin–FAK axis as a key regulator of RB progression and highlight B4GALT3 inhibition as a promising therapeutic strategy for advanced RB.