详细信息
Apoptosis, ferroptosis, and the autophagy paradox in peritoneal metastasis ( SCI-EXPANDED收录)
文献类型:期刊文献
英文题名:Apoptosis, ferroptosis, and the autophagy paradox in peritoneal metastasis
作者:Qi, Jinfeng[5];Li, Junliang[1,2,3];Wang, Ruipeng[3];Deng, Yuanyuan[4]
第一作者:Qi, Jinfeng
通信作者:Deng, YY[1]
机构:[1]Gansu Univ Chinese Med, Sch Clin Med 1, Lanzhou 730030, Peoples R China;[2]Gansu Prov Hosp, Dept Gen Surg, Lanzhou 730030, Peoples R China;[3]Lanzhou Univ, Sch Clin Med 1, Lanzhou 730030, Peoples R China;[4]Lanzhou Univ, Hosp 1, Dept Intens Care Unit, Lanzhou 730030, Peoples R China;[5]Shandong Univ, Qilu Hosp 2, Dept Gastroenterol, Jinan 250033, Peoples R China
第一机构:甘肃中医药大学
通信机构:[1]corresponding author), 1 Donggang West Rd, Lanzhou 730030, Gansu, Peoples R China.
年份:2025
卷号:275
外文期刊名:PATHOLOGY RESEARCH AND PRACTICE
收录:;WOS:【SCI-EXPANDED(收录号:WOS:001592356700001)】;
基金:This work was supported by the Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences (No. 2019PT320005, NHCDP2022028), Key Laboratory of Molecular Diagnostics and Precision Medicine for Surgical Oncology in Gansu Province (No. 2020GSZDSYS02), the Research Fund Project of Gansu Provincial Hospital (No. 22GSSYC-1, 22GSSYB-14), and Internal Project of the First Hospital of Lanzhou University (No. 2021-52).
语种:英文
外文关键词:Peritoneal metastasis; Apoptosis; Ferroptosis; Autophagy; Tumor microenvironment
摘要:Peritoneal metastasis (PM) correlates with a diminished prognosis. Throughout the progression of PM, programmed cell death (PCD) often functions as the body's defense mechanism to eliminate aberrant malignant cells. Paradoxically, PCD within tumor cell populations also holds the potential to exert a pro-cancer effect by modulating the tumor microenvironment (TME). Apoptosis-mediated innate immune cells may orchestrate the pro-cancer TME and could potentially evade cancer therapy. This discussion delineates the impacts of PCD in PM, particularly focusing on apoptosis, ferroptosis, and autophagy, constituting a "double paradox" process. On one hand, PM is restrained through the removal of cancer cells, while on the other hand, it is propelled by the stimulation of repair and regenerative responses in the TME. Furthermore, the interplay of various PCDs such as cell apoptosis, autophagy, and ferroptosis in PM is explored, alongside a summary of PCD-based anticancer strategies. These insights aim to provide a theoretical basis for the prevention and treatment of PM.
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