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<p>Clear cell renal carcinoma (ccRCC) is a prevalent kidney cancer with limited effective biomarkers for prognosis and treatment guidance. Despite advancements, a significant portion of ccRCC cases progress to advanced stages, necessitating novel diagnostic tools. Here, we investigated the expression of MUC1 and its soluble form, CA15-3, in ccRCC, evaluating their potential as biomarkers for angiogenesis and response to sunitinib therapy. Molecular analyses showed that MUC1 expression was associated with angiogenesis, epithelial–mesenchymal transition, hypoxia/metabolism regulation, and complement system activation. In particular MUC1 overexpression correlated with increased microvascular density in vitro and in vivo models. Elevated CA15-3 levels were associated with tumor burden and predict clinical response to sunitinib in metastatic ccRCC. Metabolomic analysis showed that sunitinib-responding tumors were characterized by specific metabolic changes involving glucose and lipid metabolism, in association with impaired oxidative phosphorylation. MUC1 expressing ccRCC is a high angiogenic tumor that presents characteristics of increased aggressiveness, and a specific metabolic profile. Serum CA15-3 is a marker of poor survival and predicts response of sunitinib in patients with metastatic disease.</p>

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MUC1/CA15-3 identifies a clear cell renal carcinoma characterized by Sunitinib response with a specific metabolic signature

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月14日

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  • Giuseppe Lucarelli,
  • Francesco Lasorsa,
  • Martina Milella,
  • Antonio d’Amati,
  • Giuseppe Ingravallo,
  • Antonio Di Bari,
  • Savio Domenico Pandolfo,
  • Roberto Tamma,
  • Michela De Giorgis,
  • Domenico Ribatti,
  • Annalisa Schirinzi,
  • Francesca di Serio,
  • Alessandro Caniglia,
  • Francesco Alfredo Zito,
  • Emanuele Naglieri,
  • Michele Battaglia,
  • Pasquale Ditonno,
  • Monica Rutigliano

摘要

Clear cell renal carcinoma (ccRCC) is a prevalent kidney cancer with limited effective biomarkers for prognosis and treatment guidance. Despite advancements, a significant portion of ccRCC cases progress to advanced stages, necessitating novel diagnostic tools. Here, we investigated the expression of MUC1 and its soluble form, CA15-3, in ccRCC, evaluating their potential as biomarkers for angiogenesis and response to sunitinib therapy. Molecular analyses showed that MUC1 expression was associated with angiogenesis, epithelial–mesenchymal transition, hypoxia/metabolism regulation, and complement system activation. In particular MUC1 overexpression correlated with increased microvascular density in vitro and in vivo models. Elevated CA15-3 levels were associated with tumor burden and predict clinical response to sunitinib in metastatic ccRCC. Metabolomic analysis showed that sunitinib-responding tumors were characterized by specific metabolic changes involving glucose and lipid metabolism, in association with impaired oxidative phosphorylation. MUC1 expressing ccRCC is a high angiogenic tumor that presents characteristics of increased aggressiveness, and a specific metabolic profile. Serum CA15-3 is a marker of poor survival and predicts response of sunitinib in patients with metastatic disease.