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Background <p>Tumor initiation and progression are dynamically regulated by multiple programmed cell death (PCD) pathways. In recent years, beyond apoptosis, novel cell death modalities including necroptosis, pyroptosis, ferroptosis, autophagy cell death, and cuproptosis have been shown to exhibit dual pro-tumorigenic and anti-tumorigenic effects.</p> Main Body <p>Earlier research primarily focused on their anti-cancer potential through tumor cell elimination; however, emerging evidence reveals that under specific tumor microenvironmental (TME) conditions or genetic contexts, these cell death modalities may indirectly promote immune evasion, metastatic dissemination, and therapeutic resistance. These effects are mediated through the release of damage-associated molecular patterns, which activate inflammatory responses, recruit immunosuppressive cells, and remodel stromal components, thereby accelerating malignant tumor progression.</p> Conclusion <p>This review highlights the translational potential of inhibitors targeting novel cell death modalities, such as the necroptosis inhibitor necrostatin-1, the pyroptosis inhibitor dimethyl fumarate, and the ferroptosis inhibitor ferrostatin-1, in anti-tumor therapy, providing theoretical foundations and novel perspectives for improving patient prognosis.</p>

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Programmed cell death inhibitors: a new hope for cancer therapy?

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月10日

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  • Yuting Zhong,
  • Yuan Zhang,
  • Lei Cheng,
  • Qirun Chen,
  • Guobing Zhang,
  • Zixue Xuan

摘要

Background

Tumor initiation and progression are dynamically regulated by multiple programmed cell death (PCD) pathways. In recent years, beyond apoptosis, novel cell death modalities including necroptosis, pyroptosis, ferroptosis, autophagy cell death, and cuproptosis have been shown to exhibit dual pro-tumorigenic and anti-tumorigenic effects.

Main Body

Earlier research primarily focused on their anti-cancer potential through tumor cell elimination; however, emerging evidence reveals that under specific tumor microenvironmental (TME) conditions or genetic contexts, these cell death modalities may indirectly promote immune evasion, metastatic dissemination, and therapeutic resistance. These effects are mediated through the release of damage-associated molecular patterns, which activate inflammatory responses, recruit immunosuppressive cells, and remodel stromal components, thereby accelerating malignant tumor progression.

Conclusion

This review highlights the translational potential of inhibitors targeting novel cell death modalities, such as the necroptosis inhibitor necrostatin-1, the pyroptosis inhibitor dimethyl fumarate, and the ferroptosis inhibitor ferrostatin-1, in anti-tumor therapy, providing theoretical foundations and novel perspectives for improving patient prognosis.