Aims/IntroductionThere has been conflicting evidence regarding the role of prediabetes as a risk factor of lung cancer. A systemic review and meta‐analysis was conducted to determine the relationship between prediabetes and lung cancer incidence and mortality in general adult populations.Materials and MethodsObservational studies relevant to the objective were found in Medline, Embase, Cochrane Library, and Web of Science. By incorporating potential heterogeneity into the model, a randomized‐effects model was selected.ResultsTen cohort studies were included. People with prediabetes were associated with a mildly increased risk of lung cancer incidence compared with controls with normoglycemia (risk ratio [RR]: 1.09, 95% confidence interval [CI]: 1.01–1.18, P = 0.03; I2 = 79%), which was mainly observed in men rather than in women (RR: 1.07 vs 0.99, P for subgroup difference < 0.001). Prediabetes was related to a higher risk of lung cancer mortality (RR: 1.19, 95% CI: 1.02–1.39, P = 0.03; I2 = 52%), and the results were consistent in both men and women (P for subgroup difference = 0.67). The association between prediabetes and lung cancer incidence or mortality did not appear to be significantly affected by different definitions of prediabetes (P for subgroup difference = 0.27 and 0.37).ConclusionsPrediabetes might be associated with a mildly increased risk of lung cancer incidence in men, but not in women. In addition, prediabetes may be related to a higher risk of lung cancer mortality in the adult population.

Background Colonic malignant tumor cells can cause metabolic changes in the harsh microenvironment. Glutathione reductase (GSR) plays a key role in anti-oxidative stress in tumor cells, but its specific mechanism remains unclear. Therefore, the objective of this study was to investigate the prognostic value of GSR in patients with colon cancer and its effect on tumor microenvironment. Methods Differential proteins of colon cancer and normal intestinal tissues were obtained by proteomic differential analysis, and key proteins in metabolic pathways were identified by enrichment analysis and protein-protein interaction network (PPI) analysis. Survival analysis, immune infiltration analysis and clinical information correlation analysis were performed. Results A total of 1209 differentially expressed proteins were identified in 10 colon cancer samples. GO and KEGG enrichment analysis showed that differential proteins were significantly enriched in metabolic pathways, with 144 enriched genes (p < 0.05). PPI analysis showed that ADH1A, ADH1B, ADH1C, ADH5, ALDH18A1, ALDH3A1, GSTA1, GSTA2, HPGDS and GSR were the key proteins in the differential proteins metabolic pathway of colon cancer. GEPIA2 survival analysis showed that GSR significantly affected overall survival of colon cancer patients (p = 0.0017, HR = 0.45). Timer and TISIDB database analysis showed that the expression of GSR in colon cancer can significantly affect the level of immune cell infiltration. UALCAN database analysis showed that GSR expression predicted better N stage, overall stage and lower TP53 mutation rate of colon cancer (p < 0.05). The results of HPA database analysis suggested that GSR was mainly expressed in the cytoplasm and nuclear membrane of colonic malignant tumor cells. Conclusions Our study found that GSR plays an important role in the metabolic pathway of colon cancer and affects the prognosis of patients with statistical significance. GSR significantly affects the tumor immune microenvironment, clinical stage and TP53 mutation rate of colonic malignancies. This study provides some basis for the mechanism research and treatment of colon malignancy.