Scholarlink

<p>Bladder cancer (BC) is a common urinary-tract malignancy that, once it progresses to the muscle‐invasive form (MIBC), adopts a markedly more aggressive behavior and is linked to significantly poorer patient outcomes. Despite extensive investigation, the molecular drivers of MIBC progression have yet to be fully elucidated. In this study, we demonstrate that IGF2BP3 is markedly upregulated, whereas PPARγ is significantly downregulated, in MIBC tissues compared with non–muscle–invasive disease, and that these reciprocal expression changes correlate with enhanced muscle invasion and adverse clinical outcomes. Comprehensive in vitro analyses reveal that elevated IGF2BP3 modulates BC cell motility, with overexpression enhancing migration and invasion and knockdown reducing these processes, while effects on proliferation and apoptosis were minimal. Mechanistic investigations further indicate that IGF2BP3 manipulation in vitro modulates PPARγ mRNA levels and PPARγ knockdown or overexpression respectively augments or abrogates IGF2BP3‐driven cell motility. Collectively, our findings define a novel IGF2BP3/PPARγ signaling axis that contributes to the aggressive behavior of MIBC and suggest that targeting this pathway may offer new avenues for therapeutic intervention.</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

IGF2BP3 promotes the muscle invasion of bladder cancer via PPARγ dysregulation

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月5日

查看全文
  • Jing-yi Cao,
  • Hua Peng,
  • Guang-yue Wang,
  • Ping-An Chang,
  • Wen-Tao Yao,
  • Qian Wang,
  • Jie-Zhou,
  • Gui-hua Zhang,
  • Heng Wang,
  • Jia-Cheng Wu,
  • Sha-Sha Li,
  • Quan-lan Gao,
  • Chang-song Pei,
  • Qi-chao Wang

摘要

Bladder cancer (BC) is a common urinary-tract malignancy that, once it progresses to the muscle‐invasive form (MIBC), adopts a markedly more aggressive behavior and is linked to significantly poorer patient outcomes. Despite extensive investigation, the molecular drivers of MIBC progression have yet to be fully elucidated. In this study, we demonstrate that IGF2BP3 is markedly upregulated, whereas PPARγ is significantly downregulated, in MIBC tissues compared with non–muscle–invasive disease, and that these reciprocal expression changes correlate with enhanced muscle invasion and adverse clinical outcomes. Comprehensive in vitro analyses reveal that elevated IGF2BP3 modulates BC cell motility, with overexpression enhancing migration and invasion and knockdown reducing these processes, while effects on proliferation and apoptosis were minimal. Mechanistic investigations further indicate that IGF2BP3 manipulation in vitro modulates PPARγ mRNA levels and PPARγ knockdown or overexpression respectively augments or abrogates IGF2BP3‐driven cell motility. Collectively, our findings define a novel IGF2BP3/PPARγ signaling axis that contributes to the aggressive behavior of MIBC and suggest that targeting this pathway may offer new avenues for therapeutic intervention.