Scholarlink

<p>Renal cell carcinoma (RCC) is a highly malignant tumor with a poor prognosis, underscoring the urgent need for novel therapeutic strategies. RCC cells exhibit rapid proliferation and high metabolic demands, leading to hypoglycemic and hypoxic conditions within the tumor microenvironment (TME). Our study reveals that the fructose transporter Glut5 is prominently expressed in RCC, facilitating increased fructose uptake. This compensatory mechanism supports RCC survival under glucose deprivation and hypoxia. Fructose utilization sustains RCC proliferation, migration, and colony formation in vitro, significantly reduces apoptosis, and accelerates renal cancer growth in vivo. Mechanistically, fructose activates the cAMP/PKA signaling pathway, driving metabolic reprogramming and promoting tumor progression. Furthermore, 2,5-dehydro-D-mannitol (2,5-AM), a competitive inhibitor of fructose transport, significantly inhibits RCC growth both in vivo and in vitro. These findings provide new insights into the role of fructose metabolism in RCC progression and suggest potential therapeutic targets.</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

Role of fructose in renal cell carcinoma progression

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年5月23日

查看全文
  • Jixuan Miao,
  • Di Wang,
  • Ruochong Pang,
  • Hao Zhang,
  • Yuyun Wu,
  • Xingwei Sun,
  • Yong Jin

摘要

Renal cell carcinoma (RCC) is a highly malignant tumor with a poor prognosis, underscoring the urgent need for novel therapeutic strategies. RCC cells exhibit rapid proliferation and high metabolic demands, leading to hypoglycemic and hypoxic conditions within the tumor microenvironment (TME). Our study reveals that the fructose transporter Glut5 is prominently expressed in RCC, facilitating increased fructose uptake. This compensatory mechanism supports RCC survival under glucose deprivation and hypoxia. Fructose utilization sustains RCC proliferation, migration, and colony formation in vitro, significantly reduces apoptosis, and accelerates renal cancer growth in vivo. Mechanistically, fructose activates the cAMP/PKA signaling pathway, driving metabolic reprogramming and promoting tumor progression. Furthermore, 2,5-dehydro-D-mannitol (2,5-AM), a competitive inhibitor of fructose transport, significantly inhibits RCC growth both in vivo and in vitro. These findings provide new insights into the role of fructose metabolism in RCC progression and suggest potential therapeutic targets.