LncRNA THUMPD3-AS1 promotes invasion and EMT in gastric cancer by regulating the miR-1297/BCAT1 pathway.

Long noncoding RNA (lncRNA) plays crucial roles in the development of gastric cancer (GC); however, studies of their mechanisms of action are needed to determine their clinical value. The aim of this study is to explore the effects and mechanisms of THUMPD3-AS1 in GC. Elevated levels of THUMPD3-AS1 were observed in GC and demonstrated a significant positive correlation with poor prognosis. Functionally, THUMPD3-AS1 promoted GC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) and induced tumor growth in vivo. THUMPD3-AS1 exerts its regulatory function on BCAT1 through competitive binding with miR-1297. Further investigations confirmed that both THUMPD3-AS1 and miR-1297 interact with BCAT1. These findings suggest that THUMPD3-AS1 promotes GC invasion and EMT by regulating the miR-1297/BCAT1 pathway, indicating that THUMPD3-AS1 may serve as a biomarker and therapeutic target for GC.

Erratum: LncRNA THUMPD3-AS1 promotes invasion and EMT in gastric cancer by regulating the miR-1297/BCAT1 pathway.

[This corrects the article DOI: 10.1016/j.isci.2023.107673.].

Advances in the Mechanism of Action of Neutrophil Extracellular Traps in Gastrointestinal Tumors: A Review.

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.

The Regulatory Mechanism and Research Progress of Ferroptosis in Gastric Cancer.

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.

Targeting regulatory T cells in gastric cancer: Pathogenesis, immunotherapy, and prognosis.

Gastric cancer (GC) remains one of the most common malignancies worldwide. Despite immune-checkpoint inhibitors (ICIs) has revolutionized cancer treatment and obtained durable clinical responses, only a fraction of GC patients benefit from it. As an important component of T cells, regulatory T cells (Tregs) play a vital role in the pathogenesis of GC, keep a core balance between immune suppression and autoimmunity, and function as predictive biomarkers for prognosis of GC patients. In this review, we discuss the role of Tregs in the pathogenesis of GC, and targeting Tregs via influencing their transcription factor, migration, co-stimulatory receptors, immune checkpoints, and cytokines. We also focus on the currently important findings of Tregs metabolism including amino acid, fatty acid, and lactic acid metabolism of GC. The emerging role of microbiome and clinical combined therapy in modulating Tregs in GC treatment is also summarized. Meanwhile, this review recapitulates a novel regulator, magnesium, is involved in mediating Tregs in GC. These research advances on Treg-related strategies provide new insights and challenges for GC progression, treatment, and prognosis. And we hope our review can stimulate further discovery and implication of mediators and pathways targeting Tregs.