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<p>Cancer immunotherapy has markedly improved patient outcomes, particularly when combined with conventional treatments such as chemotherapy, radiotherapy, and targeted therapy. Following these therapies, however, a subset of cancer cells can enter a senescent state, ceasing proliferation while remaining metabolically active and persistent within tissues. Such therapy-induced senescent cancer cells (TISCCs) significantly influence antitumor immune responses. TISCCs can enhance tumor immunogenicity by presenting neoantigens and activating innate immune pathways. Conversely, they can also promote T-cell immune evasion and therapeutic resistance, ultimately leading to an immunosuppressive tumor microenvironment. This dual role of TISCCs represents a critical determinant of immunotherapy efficacy, making their precise modulation a major challenge for optimizing combination treatment strategies. In this review, we comprehensively examine the opposing roles of TISCCs in antitumor immunity and highlight emerging therapeutic approaches that mitigate TISCC-driven immune suppression and improve the overall efficacy of immunotherapy-based combination regimens.</p>

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Therapy-induced senescent cancer cells as bidirectional regulators of antitumor immunity and resistance in the tumor microenvironment

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月1日

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  • Minji Choi,
  • Daeun Lee,
  • Wen-Hao Yang,
  • Jong-Ho Cha

摘要

Cancer immunotherapy has markedly improved patient outcomes, particularly when combined with conventional treatments such as chemotherapy, radiotherapy, and targeted therapy. Following these therapies, however, a subset of cancer cells can enter a senescent state, ceasing proliferation while remaining metabolically active and persistent within tissues. Such therapy-induced senescent cancer cells (TISCCs) significantly influence antitumor immune responses. TISCCs can enhance tumor immunogenicity by presenting neoantigens and activating innate immune pathways. Conversely, they can also promote T-cell immune evasion and therapeutic resistance, ultimately leading to an immunosuppressive tumor microenvironment. This dual role of TISCCs represents a critical determinant of immunotherapy efficacy, making their precise modulation a major challenge for optimizing combination treatment strategies. In this review, we comprehensively examine the opposing roles of TISCCs in antitumor immunity and highlight emerging therapeutic approaches that mitigate TISCC-driven immune suppression and improve the overall efficacy of immunotherapy-based combination regimens.