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癌症中的炎性小体与自噬:开启靶向治疗

Inflammasomes and autophagy in cancer: unlocking targeted therapies.

作者信息

Gupta Jitendra, Mohammed Mohammed Hashim, Alghazali Tawfeeq, Uthirapathy Subasini, R Roopashree, Thakur Vishal, Kaur Manpreet, Naidu K Satyam, Kubaev Aziz, Al-Mukhtar Mahmoud Mussleh

机构信息

Institute of Pharmaceutical Research, GLA University, Mathura, Pin Code 281406, U.P., India.

Medical Laboratory Techniques Department, College of Health and Medical Technology, Al-Maarif University, Anbar, Iraq.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 2025 May 1. doi: 10.1007/s00210-025-04184-x.

Abstract

This study clarifies the interaction between autophagy and inflammasome within the cancer framework. The inflammasome generates pro-inflammatory cytokines to direct the immune response to pathogens and cellular stressors. Autophagy maintains cellular homeostasis and can either promote or inhibit cancer. These pathways interact to affect tumorigenesis, immune responses, and therapy. Autophagy controls inflammasome activity by affecting cancer pathogenesis and tumor microenvironment inflammation, highlighting novel cancer therapeutic approaches. Recent studies indicate that modulating autophagy and inflammasome pathways can boost anti-cancer immunity, reduce drug-resistance, and improve therapeutic efficacy. Recent studies indicate modulating inflammasome and autophagy pathways can augment anti-cancer immunity, mitigate therapy resistance, and improve treatment efficacy. Cancer research relies on understanding the inflammasome-autophagy relationship to develop targeted therapies that enhance anti-tumor efficacy and reduce inflammatory symptoms. Customized therapies may improve outcomes based on autophagy gene variations and inflammasome polymorphisms. This study investigates autophagy pathways and the inflammasome in tumor immunopathogenesis, cytokine function, and cancer therapeutic strategies, highlighting their significance in cancer biology and treatment.

摘要

本研究阐明了癌症框架内自噬与炎性小体之间的相互作用。炎性小体产生促炎细胞因子,以指导针对病原体和细胞应激源的免疫反应。自噬维持细胞稳态,既可以促进也可以抑制癌症。这些途径相互作用,影响肿瘤发生、免疫反应和治疗。自噬通过影响癌症发病机制和肿瘤微环境炎症来控制炎性小体活性,突出了新的癌症治疗方法。最近的研究表明,调节自噬和炎性小体途径可以增强抗癌免疫力、降低耐药性并提高治疗效果。最近的研究表明,调节炎性小体和自噬途径可以增强抗癌免疫力、减轻治疗耐药性并提高治疗效果。癌症研究依赖于理解炎性小体 - 自噬关系,以开发增强抗肿瘤疗效并减轻炎症症状的靶向疗法。基于自噬基因变异和炎性小体多态性的定制疗法可能会改善治疗结果。本研究调查了肿瘤免疫发病机制、细胞因子功能和癌症治疗策略中的自噬途径和炎性小体,突出了它们在癌症生物学和治疗中的重要性。

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