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<p>Cancer relapse upon chemotherapy remains the primary challenge in cancer treatment. By integrating high-resolution CRISPR/Cas9-based evolving lineage tracing with single-cell RNA sequencing in mice, we track the evolution of bladder carcinoma in the presence or absence of chemotherapy. We find that a cell population exhibiting an epidermoid-like cell state can survives chemotherapy. These epidermoid-like cells leave the quiescent state to initiate relapse, generating histologically distinct tumours through different evolutionary routes involving specific transcriptional changes. The plasticity of epidermoid-like cells and alterations in plasticity patterns during evolution shape the phenotypes of relapsed tumours. Integrated analyses reveal that Insulin-like growth factor-binding protein 5 is a key co-regulator of aggressive progression and squamous features in bladder carcinoma. Impeding insulin-like growth factor-binding protein 5 expression suppresses the chemoresistance and malignant behaviours of relapsed tumours. Our study deciphers key events and evolutionary dynamics during the natural progression and recurrence of bladder carcinoma. It offers a viable therapeutic approach to overcome the refractoriness of relapsed bladder carcinoma to conventional chemotherapy.</p>

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Recurrence in the chemotherapy regimen of bladder carcinoma originates from quiescent epidermoid-like cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月27日

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  • Dewang Zhou,
  • Yuqing Li,
  • Zeqin Yan,
  • Jianxu Huang,
  • Yishu Bao,
  • Chunyang Gao,
  • Caiting Tang,
  • Xinchen Wu,
  • Shang Wang,
  • Daitian Tang,
  • Haoxiang Zheng,
  • Weihan Luo,
  • Fei Li,
  • Weibiao Ye,
  • Zhaohua Ye,
  • Xiqi Peng,
  • Yujun Liu,
  • Shimao Zhu,
  • Yang Du,
  • Jean Paul Thiery,
  • Song Wu

摘要

Cancer relapse upon chemotherapy remains the primary challenge in cancer treatment. By integrating high-resolution CRISPR/Cas9-based evolving lineage tracing with single-cell RNA sequencing in mice, we track the evolution of bladder carcinoma in the presence or absence of chemotherapy. We find that a cell population exhibiting an epidermoid-like cell state can survives chemotherapy. These epidermoid-like cells leave the quiescent state to initiate relapse, generating histologically distinct tumours through different evolutionary routes involving specific transcriptional changes. The plasticity of epidermoid-like cells and alterations in plasticity patterns during evolution shape the phenotypes of relapsed tumours. Integrated analyses reveal that Insulin-like growth factor-binding protein 5 is a key co-regulator of aggressive progression and squamous features in bladder carcinoma. Impeding insulin-like growth factor-binding protein 5 expression suppresses the chemoresistance and malignant behaviours of relapsed tumours. Our study deciphers key events and evolutionary dynamics during the natural progression and recurrence of bladder carcinoma. It offers a viable therapeutic approach to overcome the refractoriness of relapsed bladder carcinoma to conventional chemotherapy.