Scholarlink

<p>Renal cell carcinoma (RCC) undergoes profound metabolic reprogramming to fuel its aggressive progression and metastatic dissemination. While transketolase (TKT), a central metabolic enzyme, has been shown to exert dichotomous roles as either oncogenic or tumor-suppressive factors across different malignancies, its functional significance in RCC pathogenesis remains inadequately defined. In this study, we demonstrate that TKT promotes glucose metabolism in RCC by enhancing glycolysis, thereby supporting tumor progression. TKT expression is significantly elevated in RCC tissues and correlates with poor patient prognosis. Mechanistically, we uncovered a novel functional axis between TKT and the glycolytic gatekeeper pyruvate kinase M2 (PKM2), where their coordinated action drives metastatic progression and metabolic adaptation in RCC. Knockdown of PKM2 significantly impaired the TKT-mediated increases in glycolysis, cell proliferation, and invasive potential. Taken together, our findings highlight TKT as a pivotal regulator of metabolic reprogramming in RCC and suggest its potential as a therapeutic target for the treatment of this malignancy.</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

TKT drives renal cell carcinoma progression through metabolic reprogramming and synergistic interaction with PKM2

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月18日

查看全文
  • Qianqing Wang,
  • Anqun Tang,
  • Qingxin Zhuang,
  • Haifeng Xu,
  • Shiping Xu,
  • Jing Zhang,
  • Yao Wang,
  • Liantao Li,
  • Sufang Chu,
  • Yan Wang,
  • Jin Bai,
  • Minle Li,
  • Rui Zhang

摘要

Renal cell carcinoma (RCC) undergoes profound metabolic reprogramming to fuel its aggressive progression and metastatic dissemination. While transketolase (TKT), a central metabolic enzyme, has been shown to exert dichotomous roles as either oncogenic or tumor-suppressive factors across different malignancies, its functional significance in RCC pathogenesis remains inadequately defined. In this study, we demonstrate that TKT promotes glucose metabolism in RCC by enhancing glycolysis, thereby supporting tumor progression. TKT expression is significantly elevated in RCC tissues and correlates with poor patient prognosis. Mechanistically, we uncovered a novel functional axis between TKT and the glycolytic gatekeeper pyruvate kinase M2 (PKM2), where their coordinated action drives metastatic progression and metabolic adaptation in RCC. Knockdown of PKM2 significantly impaired the TKT-mediated increases in glycolysis, cell proliferation, and invasive potential. Taken together, our findings highlight TKT as a pivotal regulator of metabolic reprogramming in RCC and suggest its potential as a therapeutic target for the treatment of this malignancy.