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<p>Bladder cancer (BLCA) is the most prevalent malignant tumor of the urinary system. Mitophagy is a selective form of autophagy that occurs within the mitochondria. The goal of this study was to determine mitophagy-related biomarkers associated with BLCA and to explore their underlying molecular mechanisms. CTSK, MTERF3, SRC, and CSNK2B were identified as biomarkers. A risk model classified BLCA patients into high-risk group (HRG) and low-risk group (LRG), with HRG patients exhibiting lower survival probabilities. The “chemical carcinogenesis-DNA adducts” and “cytokine-cytokine receptor interaction” signaling pathway were closely associated with HRG and LRG. TP53 had the highest mutation frequencies in the HRG and LRG, respectively. The two groups exhibited significant differences in 14 immune cells, including M2 macrophages. CTSK exhibited the strongest correlation with the naive B cells. A total of 135 drugs differed in sensitivity between HRG and LRG, including KU.55933. The identified regulatory network included ADAMTSL4-AS1-hsa-miR-149-5p-SRC. Expression analysis showed that CTSK was significantly downregulated in the BLCA group, while MTERF3, SRC, and CSNK2B were significantly upregulated. In conclusion, CTSK, MTERF3, SRC, and CSNK2B laid the foundation for targeted therapy in the treatment of BLCA.</p>

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Identification of biomarkers associated with mitophagy in bladder cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月26日

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  • Xianbin Huang,
  • Yanqiu Meng,
  • Jielong Song,
  • Yizi Zhu,
  • Jian Li,
  • Yan Xi,
  • Xiaodong Peng,
  • Yaoyi Xiong

摘要

Bladder cancer (BLCA) is the most prevalent malignant tumor of the urinary system. Mitophagy is a selective form of autophagy that occurs within the mitochondria. The goal of this study was to determine mitophagy-related biomarkers associated with BLCA and to explore their underlying molecular mechanisms. CTSK, MTERF3, SRC, and CSNK2B were identified as biomarkers. A risk model classified BLCA patients into high-risk group (HRG) and low-risk group (LRG), with HRG patients exhibiting lower survival probabilities. The “chemical carcinogenesis-DNA adducts” and “cytokine-cytokine receptor interaction” signaling pathway were closely associated with HRG and LRG. TP53 had the highest mutation frequencies in the HRG and LRG, respectively. The two groups exhibited significant differences in 14 immune cells, including M2 macrophages. CTSK exhibited the strongest correlation with the naive B cells. A total of 135 drugs differed in sensitivity between HRG and LRG, including KU.55933. The identified regulatory network included ADAMTSL4-AS1-hsa-miR-149-5p-SRC. Expression analysis showed that CTSK was significantly downregulated in the BLCA group, while MTERF3, SRC, and CSNK2B were significantly upregulated. In conclusion, CTSK, MTERF3, SRC, and CSNK2B laid the foundation for targeted therapy in the treatment of BLCA.