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Lung cancer is one of the most common cancers in the world, and its treatment strategy is mainly surgery combined with radiotherapy and chemotherapy. However, long-term chemotherapy will result in drug resistance, which is also one of the difficulties in the treatment of lung cancer. Ferroptosis is an iron-dependent and lipid peroxidation-driven non-apoptotic cell death cascade, occurring when there is an imbalance of redox homeostasis in the cell. Nuclear factor erythroid 2-related factor 2 (Nrf2) is key for cellular antioxidant responses. Numerous studies suggest that Nrf2 assumes an extremely important role in regulation of ferroptosis, for its various functions in iron, lipid, and amino acid metabolism, and so on. In this review, a brief overview of the research progress of ferroptosis over the past decade will be presented. In particular, the mechanism of ferroptosis and the regulation of ferroptosis by Nrf2 will be discussed, as well as the role of the Nrf2 pathway and ferroptosis in tumor drug resistance, which will provide new research directions for the treatment of drug-resistant lung cancer patients.
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The morbidity and mortality of lung cancer ranks among the top cancers in the world. Non-small cell lung cancer (NSCLC) is the main pathological type of lung cancer, with limited treatment options and poor prognosis. The nuclear factor E2-related factor 2 (NRF2) signaling pathway is highly mutated and activated in NSCLC, and promotes the malignant progression of lung cancer through various mechanisms. NRF2-targeted therapy will provide new treatment strategies for patients with NSCLC. This article will review the basic structure and response pathways of the NRF2 pathway, the mechanism of NRF2 regulating lung cancer cell proliferation, and the research and development progress of NRF2 inhibitors.
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Iron metabolism is the process of absorption, transport, storage and conversion and excretion of the essential trace element iron in living organisms. Normal iron metabolism tightly regulates iron content at the systemic and cellular levels through a variety of related proteins to prevent excessive free radicals from being generated during the iron cycle that can damage the body. Various abnormalities in iron metabolism are found in a variety of lymphohaematopoietic tumours and an insidious link between iron metabolism and tumour development has been revealed. Serum ferritin levels and abnormalities of iron transport proteins, transferrin and their receptors can be used as prognostic indicators for lymphohematopoietic tumours and have opened up new directions of diagnosis and treatment, with a large number of novel drugs targeting tumours emerging to date. This article briefly describes the normal iron metabolism process and highlights the progress of research on abnormal iron metabolism in lymphohematopoietic tumors at the systemic and cellular levels.

Objective To explore the molecular mechanism underlying gastric carcinogenesis and progression by using gene expression profiling array together with bioinformatics. Methods Lentivirus short hairpin RNA targeting STIL(ShSTIL)and scrambled sequence RNA(ShCon)were transduced into the gastric cancer cell line SGC-7901.RNA extraction,complementary DNA synthesis,construction of biotin-labelled amplified RNA probes,and hybridization with gene expression profile were consecutively performed.We collected corresponding data and analyzed differentially expressing genes(DEGs),followed by the analysis of gene ontology(GO)and Kyoto encyclopedia of genes and genomes(KEGG)enrichment,transcription factor regulating network,and protein-protein interacting networks. Results Compared with ShCon,a total of 417 and 87 genes were respectively down-regulated and up-regulated,respectively,in the ShSTIL group( P <0.05,fold change>1 or <-1).GO and KEGG enrichment analysis indicated that genes regulated by STIL were localized in cytoplasm,extracellular exosome,Golgi apparatus and various biomembranes,and were implicated in the ubiquitin-mediated proteolysis,P53 signaling pathway,and pathways regulating pluripotency of stem cells.Evaluation on genes enriched in KEGG pathways,regulation of transcription factors,and protein-protein interacting network demonstrated that IGF1R,STUB1,SKP2,and FOXO1 were localized at the centre of the network and played a key role in the development and progression of gastric cancer. Conclusion Through the protein-protein interactions,STIL may activate E3 ubiquitin ligase STUB1 or SKP2,promote the proteolysis of FOXO1-a transcription factor,regulate the expression of IGF1R,and thus promote gastric carcinogenesis and progression.

Objective: To investigate changes of vWF in vascular endothelial cells with acute hypoxia and assess its significance in the study of vascular injury and hypercoagulability., Methods: vWF in vascular endothelial cells and in blood were measured by immunohistochemical staining image analysis and ELISA technique. Fibrin was displayed by phosphotungstic hematoxylin staining., Results: The amount of vWF in vascular endothelial cells decreased progressively, while in blood increased progressively with hypoxia. Fibrin prominently increased with hypoxia., Conclusion: Acute hypoxia caused severe injury of vascular endothelial cells which resulted in release of vWF into blood from endothelial cells. The vWF amounts in blood may reflect the hypercoagulability, and may serve as a useful indicator of vascular injury and hypercoagulability.