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Programmed cell death inhibitors: a new hope for cancer therapy?
Yuting Zhong1, Yuan Zhang2,3, Lei Cheng2,3
1Center for Clinical Pharmacy, Cancer Center, Department of Pharmacy, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China.
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.
Insights
Novel programmed cell death (PCD) pathways, beyond apoptosis, can promote tumor progression by aiding immune evasion and metastasis. Inhibitors targeting these pathways offer new anti-cancer therapy strategies.
Area of Science:
- Oncology
- Cell Biology
- Immunology
Background:
- Multiple programmed cell death (PCD) pathways, including necroptosis, pyroptosis, ferroptosis, autophagy cell death, and cuproptosis, play a dual role in tumor initiation and progression.
- While initially studied for anti-cancer effects via tumor cell elimination, emerging evidence shows these PCD pathways can also promote tumor progression.
Purpose of the Study:
- To review the dual role of novel PCD modalities in cancer.
- To explore how these cell death pathways can promote tumor progression under specific conditions.
- To highlight the therapeutic potential of targeting novel PCD pathways.
Main Methods:
- Review of recent scientific literature on programmed cell death pathways in cancer.
- Analysis of mechanisms by which PCD modalities influence the tumor microenvironment (TME).
- Examination of emerging therapeutic strategies targeting novel cell death pathways.
Main Results:
- Novel PCD pathways can promote tumor progression by facilitating immune evasion, metastatic dissemination, and therapeutic resistance.
- These effects are mediated by the release of damage-associated molecular patterns (DAMPs), leading to inflammation and immunosuppression.
- Specific TME conditions and genetic contexts dictate whether PCD pathways are anti-tumorigenic or pro-tumorigenic.
Conclusions:
- Targeting novel cell death modalities with inhibitors like necrostatin-1, dimethyl fumarate, and ferrostatin-1 shows translational potential in anti-tumor therapy.
- Understanding the complex roles of PCD pathways provides new perspectives for improving patient prognosis.
- Further research into PCD inhibitors could lead to novel anti-cancer therapeutic strategies.
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