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Ferroptosis regulates key signaling pathways in gastrointestinal tumors:Underlying mechanisms and therapeutic strategies

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World Journal of Gastroenterology 2023年第16期29卷 2433-2451页

作者： Ravichandiran Rabitha Sethuraman Shivani Yahya Showket ganapasam sudhandiran Department of Biochemistry University of MadrasCell Biology Research LaboratoryChennai 600025Tamil NaduIndia

Ferroptosis is an emerging novel form of non-apoptotic,regulated cell death that is heavily dependent on iron and characterized by rupture in plasma *** is distinct from other regulated cell death modalities at the biochemical,morphological,and molecular *** ferroptotic signature includes high membrane density,cytoplasmic swelling,condensed mitochondrial membrane,and outer mitochondrial rupture with associated features of accumulation of reactive oxygen species and lipid *** selenoenzyme glutathione peroxidase 4,a key regulator of ferroptosis,greatly reduces the lipid overload and protects the cell membrane against oxidative *** exerts a momentous role in regulating cancer signaling pathways and serves as a therapeutic target in *** ferroptosis orchestrates gastrointestinal(GI)cancer signaling pathways leading to GI tumors such as colonic cancer,pancreatic cancer,and hepatocellular *** exists between ferroptosis and other cell death *** apoptosis and autophagy play a detrimental role in tumor progression,depending upon the factors associated with tumor microenvironment,ferroptosis plays a decisive role in either promoting tumor growth or suppressing *** transcription factors,such as TP53,activating transcription factors 3 and 4,are involved in influencing ***,several molecular mediators of ferroptosis,such as p53,nuclear factor erythroid 2–related factor 2/heme oxygenase-1,hypoxia inducible factor 1,and sirtuins,coordinate with ferroptosis in GI *** this review,we elaborated on key molecular mechanisms of ferroptosis and the signaling pathways that connect ferroptosis to GI tumors.

关键词： Ferroptosis Gastrointestinal cancers Nuclear factor erythroid 2-related factor 2 Apoptosis Autophagy

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Colorectal carcinogenesis:Insights into the cell death and signal transduction pathways:A review

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World Journal of Gastrointestinal Oncology 2018年第9期10卷 244-259页

作者： Ashok kumar Pandurangan Thomas Divya Kalaivani Kumar Vadivel Dineshbabu Bakthavatchalam Velavan ganapasam sudhandiran Cell Biology Laboratory Department of Bio-chemistryUniversity of MadrasGuindy Campus School of Life sciences B.S. Abdur Rahman Crescent Institute of Science and Technology

Colorectal carcinogenesis(CRC) imposes a major health burden in developing countries. It is the third major cause of cancer deaths. Despite several treatment strategies, novel drugs are warranted to reduce the severity of this disease. Adenomatous polyps in the colon are the major culprits in CRC and found in 45% of cancers, especially in patients 60 years of age. Inflammatory polyps are currently gaining attention in CRC, and a growing body of evidence denotes the role of inflammation in CRC. Several experimental models are being employed to investigate CRC in animals, which include the APC^(min/+) mouse model, Azoxymethane, Dimethyl hydrazine, and a combination of Dextran sodium sulphate and dimethyl hydrazine. During CRC progression, several signal transduction pathways are activated. Among the major signal transduction pathways are p53, Transforming growth factor beta, Wnt/β-catenin, Delta Notch, Hippo signalling, nuclear factor erythroid 2-related factor 2 and Kelch-like ECH-associated protein 1 pathways. These signalling pathways collaborate with cell death mechanisms, which include apoptosis, necroptosis and autophagy, to determine cell fate. Extensive research has been carried out in our laboratory to investigate these signal transduction and cell death mechanistic pathways in CRC. This review summarizes CRC pathogenesis and the related cell death and signal transduction pathways.

关键词： Colorectal cancer Cell death Apoptosis Autophagy Inflammation Hippo signalling Nuclear factor erythroid 2-related factor 2 Wnt signaling

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