Ferroptosis is a novel cell death modality discovered in recent years that is different from apoptosis and necrosis. It is usually associated with changes in the regulatory signaling in multiple organelles and depends on iron. It is caused by an imbalance between the generation and degradation of intracellular lipid reactive oxygen species (ROS). In addition to increased levels of cytoplasmic ROS and lipids, decreased mitochondrial volume and thickened mitochondrial membranes are markers of ferroptotic death. Gastric cancer is a common malignant tumor, but few studies on the possible role of ferroptosis in gastric cancer have been reported. Although ferroptosis is involved in multifactor-induced carcinogenesis, studies have also shown the role of ferroptosis in the selective killing of tumor cells, thereby inhibiting tumor progression and metastasis. In this paper, the definition, characteristics, and regulatory mechanism of ferroptosis and its potential role in gastric cancer are discussed. Therefore, this review is expected to provide a reference for the treatment of diseases based on ferroptosis and provide a direction for future research on the pathogenesis and development of gastric cancer and the development of anticancer drugs.

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Introduction Neutrophils are important immune cells in the body, extremely abundant, phagocytic and bactericidal, and usually involved in the defense against infectious diseases as immune become. However, a new reticulum structure has been discovered: neutrophil extracellular traps (NETs), which consists of various components such as DNA and proteins, etc. Current studies have found that NETs are closely associated with various diseases such as immune diseases, inflammation and tumors, and the study of the development and metastasis of gastrointestinal tumors has become a recent research hotspot. The clinical significance of NETs has been gradually highlighted, especially in the area of immunosuppression. Methods We reviewed a large amount of relevant literature, summarized the latest detection methods of NETs, explored the mechanism of NETs in gastrointestinal tumors and summarized the latest hotspot directions. Results NETs are involved in the development of gastrointestinal tumors, and are closely related to the proliferation and metastasis of gastrointestinal tumors. Higher levels of NETs are associated with poor prognosis of gastrointestinal tumors, promote local growth of tumors through various pathways, participate in tumor-related systemic injury, and promote tumor growth and metastasis by enhancing the mitochondrial function of tumor cells and awakening dormant tumor cells. Discussion NETs are highly expressed in tumors, and tumors and their microenvironment can promote the production of NETs, providing new ideas for the clinical diagnosis and treatment of gastrointestinal tumors. In this paper, we describe the basic information about NETs, explore the research mechanisms related to NETs in gastrointestinal tumors, and prospectively explore the clinical potential of hotspots and inhibitors related to NETs for gastrointestinal tumors, in order to provide new ideas and targets for the diagnosis and treatment of gastrointestinal tumors.

Objective Long noncoding RNAs (lncRNAs) are significant regulators in gastric cancer（GC）; However, studies of their mechanisms of action are needed to determine their clinical value. In this study, we investigated the effects and mechanism of action of THUMPD3-AS1 in GC. Methods Candidate lncRNAs and mRNAs were getted from The Cancer Genome Atlas, revealing the differential expression and prognostic significance of THUMPD3-AS1-BCAT1 in GC. qRT-PCR was performed to detect THUMPD3-AS1 levels in GC samples and cell lines. CCK8, scratch wound healing, and Transwell assays as well as experiments in vivo were conducted to evaluate the function of THUMPD3-AS1 in GC. Related genes were analysed to detect interactions between THUMPD3-AS1, BCAT1, and miR-1297. Results THUMPD3-AS1 levels were significantly elevated in GC and were positively correlated with poor prognosis. Functionally, THUMPD3-AS1 promoted GC cell proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) and induced tumour growth in vivo. THUMPD3-AS1 regulated BCAT1 by competitively binding to miR-1297; further analyses revealed that both THUMPD3-AS1 and miR-1297 can interact with BCAT1. Conclusions These findings demonstrate that THUMPD3-AS1 promotes GC cell invasion and EMT via the miR-1297/BCAT1 pathway, suggesting that THUMPD3-AS1 is a novel biomarker and therapeutic target for GC.

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