详细信息
细胞焦亡及其相关因子caspase-1和IL-1β与非小细胞肺癌
Cell pyroptosis and related factors caspase-1,IL-1β,and non-small cell lung cancer
文献类型:期刊文献
中文题名:细胞焦亡及其相关因子caspase-1和IL-1β与非小细胞肺癌
英文题名:Cell pyroptosis and related factors caspase-1,IL-1β,and non-small cell lung cancer
作者:王金霞[1];雷丰丰[2]
第一作者:王金霞
机构:[1]甘肃中医药大学第一临床医学院,兰州730030;[2]甘肃省人民医院呼吸与危重症医学科,兰州730030
第一机构:甘肃中医药大学临床医学院
年份:2024
卷号:44
期号:1
起止页码:87
中文期刊名:临床与病理杂志
外文期刊名:Journal of Clinical and Pathological Research
收录:CSTPCD
基金:国家自然科学基金(41961016)。
语种:中文
中文关键词:非小细胞肺癌;细胞焦亡;半胱天冬氨酸蛋白酶-1;白细胞介素-1β
外文关键词:non-small cell lung cancer;pyroptosis;caspase-1;interleukin 1β
摘要:细胞焦亡是一种与炎症相关的程序性细胞死亡过程,其经半胱天冬氨酸蛋白酶-1(caspase-1)与促炎因子白细胞介素-1β(interleukin 1β,IL-1β)介导后发生,从而发挥促进或抑制非小细胞肺癌(non-small cell lung cancer,NSCLC)发生、发展的双重作用。一方面,焦亡相关因子通过构建促肿瘤微环境助力NSCLC进展;另一方面,caspase-1和IL-1β通过调控经典炎性细胞焦亡途径延缓NSCLC进展。在肺肿瘤治疗方面,尽管部分化学治疗、免疫治疗、靶向治疗及中草药治疗通过细胞焦亡分子调控机制增强了药物敏感性,使癌细胞的进展得到延缓,但同时周围正常组织也因细胞焦亡产生的不良反应而受到伤害。Caspase-1、IL-1β作为新的、独立的生物学标志物可通过诱导细胞焦亡的发生而参与NSCLC的发生,并能在NSCLC治疗中发挥作用,可为NSCLC靶向治疗提供新的理论依据和策略。
Cell pyroptosis is a programmed cell death process associated with inflammation,which occurs after mediation by caspase-1 and the pro-inflammatory factor interleukin1β(IL-1β),exerting a dual role in promoting or inhibiting the occurrence and development of non-small cell lung cancer(NSCLC).On the one hand,pyroptosis and related factors contribute to the progression of NSCLC by building a pro-tumor microenvironment.On the other hand,caspase-1 and IL-1βdelay NSCLC progression by regulating the classical inflammatory pyroptosis pathway.In terms of lung tumor treatment,although some chemotherapy,immunotherapy,targeted therapy,and Chinese medicine therapy enhance drug sensitivity through the regulation of cell pyroptosis molecular mechanisms,delaying the progression of cancer cells,the surrounding normal tissues are also damaged due to adverse reactions caused by cell pyroptosis.To explore the role of caspase-1 and IL-1βas novel,independent biomarkers in the occurrence and treatment of NSCLC by inducing pyroptosis,and to provide a new theoretical basis and strategy for the targeted treatment of NSCLC.
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