胰腺癌中铁死亡的阴暗面
The dark side of ferroptosis in pancreatic cancer.
作者信息
Liu Jiao, Dai Enyong, Kang Rui, Kroemer Guido, Tang Daolin
机构信息
Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
Department of Oncology and Hematology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China.
出版信息
Oncoimmunology. 2021 Jan 4;10(1):1868691. doi: 10.1080/2162402X.2020.1868691.
Drug-induced ferroptosis, an iron-dependent regulatory necrosis, has been proposed for the therapy of pancreatic ductal adenocarcinoma. However, genetically engineered mouse models have revealed that high-iron diets or deletion of pancreatic GPX4 (a key repressor of ferroptosis) accelerate the development of mutant -driven PDAC by activating the STING1/TMEM173-dependent DNA sensor pathway. ADM: acinar-to-ductal metaplasia; CGAS: cyclic GMP-AMP synthase; DAMP: damage-associated molecular pattern; GPX4: glutathione peroxidase 4; GEMM: genetically engineered mouse models; PDAC: pancreatic ductal adenocarcinoma; PanIN: pancreatic intraepithelial neoplasia, SLC7A11: solute carrier family 7 member 11; STING1: cGAMP-stimulator of interferon response cGAMP interactor 1; TME: tumor microenvironment; 8-OHG: 8-hydroxy-2'-deoxyguanosine.
药物诱导的铁死亡是一种铁依赖性调节性坏死，已被提出用于治疗胰腺导管腺癌。然而，基因工程小鼠模型显示，高铁饮食或胰腺GPX4（铁死亡的关键抑制因子）的缺失通过激活STING1/TMEM173依赖性DNA传感途径加速了突变驱动的胰腺导管腺癌的发展。ADM：腺泡-导管化生；CGAS：环状GMP-AMP合酶；DAMP：损伤相关分子模式；GPX4：谷胱甘肽过氧化物酶4；GEMM：基因工程小鼠模型；胰腺导管腺癌；PanIN：胰腺上皮内瘤变，SLC7A11：溶质载体家族7成员11；STING1：干扰素反应cGAMP相互作用因子1的cGAMP刺激物；TME：肿瘤微环境；8-OHG：8-羟基-2'-脱氧鸟苷。
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