Background Gastrointestinal cancers account for 20% of all deaths worldwide. Gastric cancer (GC) patients are susceptible to psychological change, especially depression which is commonly induced by chronic stress. Gastric precancerous lesions (GPL) is an important prodromal stage in the occurrence of gastric cancer. Chronic stress influences the prognosis of GC and may influence the process of GPL as well. Methods Sixty SD rats were randomly divided into a control group, GPL group, and GPL+CUMS group. In the GPL group, 200μg/mL N-methyl-N’-nitro-N-nitrosoguanidine (MNNG) free drinking method combined with intermittent fasting was applied to establish the GPL animal model. Based on this, we combined the GPL rats with chronic unpredicted mild stress (CUMS) to establish a comprehensive model. We then evaluated their behavior by open field tests and sucrose preference tests. We tested the IL-6, IL-10, TNF-α, Ghrelin, Leptin and Somatostatin (SS) levels in serum and observed the expression of Ghrelin and Gastrokinof the gastric mucosa and tumor, but also had expression of Ghrelin on the luminal side of the gastric mucosa. The areas that showed strong expression of GKN2 and Ghrelin, are all located around the blood vessels in the tumor. Conclusions GPL rats under chronic stress would aggravate the conditions of GPL, shorten the process of GPL, and increase the risk of tumorigenesis. In addition, the close monitoring of the mental health of cancer survivors and precancerous lesion patients is suggested to be of great significance in the prevention and treatment of cancer.Glycosylation changes are key molecular events in tumorigenesis, progression and glycosyltransferases play a vital role in the this process. FUT8 belongs to the fucosyltransferase family and is the key enzyme involved in N-glycan core fucosylation. FUT8 and/or core fucosylated proteins are frequently upregulated in liver, lung, colorectal, pancreas, prostate,breast, oral cavity, oesophagus, and thyroid tumours, diffuse large B-cell lymphoma, ependymoma, medulloblastoma and glioblastoma multiforme and downregulated in gastric cancer. They can be used as markers of cancer diagnosis, occurrence, progression and prognosis. Core fucosylated EGFR, TGFBR, E-cadherin, PD1/PD-L1 and α3β1 integrin are potential targets for tumour therapy. In addition, IGg1 antibody defucosylation can improve antibody affinity, which is another aspect of FUT8 that could be applied to tumour therapy.Recent reports show that long noncoding RNA (lncRNA) FIRRE contributes to the proliferation, apoptosis resistance, and invasion of colorectal cancer and diffuse large B-cell lymphoma. However, the biological function of FIRRE in hepatocellular carcinoma (HCC) remains unknown. Here, we disclosed that the FIRRE level was frequently increased in HCC compared to nontumor tissues. Compared with normal liver cells, we also confirmed the upregulated level of FIRRE in HCC cells. Notably, the FIRRE high expression was related to malignant clinical features, including advanced TNM stage and tumor size ≥5 cm, and conferred to worse survival of HCC. Functionally, FIRRE knockdown repressed the proliferation and glycolysis of HCCLM3 cells. Overexpression of FIRRE strengthened Huh7 cell proliferation and glycolysis. Notably, FIRRE positively regulated the glycolic enzyme 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 (PFKFB4) expression in HCC cells. PFKFB4 was highly expressed and positively associated with FIRRE level in HCC tissues. The upregulated expression of PFKFB4 was associated with high tumor grade and advanced TNM stage. TCGA data revealed that the PFKFB4 high expression indicated a poor prognosis of HCC. Mechanistically, modulating FIRRE level did not affect the stability of PFKFB4 mRNA. FIRRE was mainly distributed in HCC cells’ nucleus and promoted PFKFB4 transcription and expression via cAMP-responsive element-binding protein (CREB). PFKFB4 could abolish the effects of FIRRE knockdown on HCC cell proliferation and glycolysis. To conclude, the highly expressed FIRRE facilitated HCC cell proliferation and glycolysis by enhancing CREB-mediated PFKFB4 transcription and expression.Background Tissue inhibitor of metalloproteinases (TIMP) gene family, including TIMP1, TIMP2, TIMP3 and TIMP4, was found to be correlated with serval cancers. Still the diagnostic and prognostic study of it in gastric cancer (GC) have few reports. Methods and materials In this study, the gene expression and clinical data were acquired from the Cancer Gene Atlas (TCGA), function enrichment was used by several databases for verifying known function. Operating characteristic (ROC) curves with area under the curve (AUC) used to assess diagnostic value. Survival analysis and joint-effects survival analysis was performed by the Kaplan-Meier curve. The results were adjusted by cox-regression model. Nomogram is used to directly predict the survival rate for individual GC patient. The potential mechanism for diagnostic and prognostic value was assessed by gene set enrichment analysis (GSEA). Further functions of gene were verified by cell proliferation, migration and invasion assays in human gastric cancer cell line. Results TIMP1 was expressed in GC tissue was higher than normal gastric tissue. selleck chemical TIMP3 and TIMP4 have expressed in normal gastric tissue were higher than GC tissue. TIMP1, TIMP3 and TIMP4 have potential diagnostic value (AUC=0.842, 0.729, 0.786 respectively; all P less then 0.01). Low expression of TIMP2 and TIMP3 associated with favorable overall survival (all P less then 0.05). TIMP2 and TIMP3, which had significantly affection of prognosis were found having some function such as tRNA processing, cell cycle pathway ncRNA processing. The silencing of TIMP3 could inhibit the migration and invasion of gastric cancer cell. Conclusion We analyzed the TIMP gene family in GC, and the prognostic and diagnostic value. TIMP1 and TIMP2 could be used as diagnostic biomarkers in GC. TIMP2 and TIMP3 could be used as potential biomarkers for GC’s prognosis.Non-small cell lung cancer (NSCLC) is one of the major cancer-related causes of morbidity and mortality worldwide. Despite the progress in lung cancer treatment, there is still an urgent need to discover novel therapeutic agents for NSCLC. Natural products represent a rich source of bioactive compounds. Through a natural compound library screening assay, we found that a group of anti-insect drugs had significant inhibitory effect on the proliferation of NSCLC cells. Among the anti-insect drugs, two derivatives of artemisinin, i.e., artesunate (ART) and dihydroartemisinin (DHA), a group of well-known anti-malarial drugs, have been shown to possess selective anti-cancer properties. Mechanistically, we found that ART and DHA induced apoptosis of A549 cells as evidenced by decreased protein level of VDAC and increased caspase 3 cleavage. Furthermore, cystine/glutamate transporter (xCT), a core negative regulator of ferroptosis, was downregulated by ART and DHA. The mRNA level of transferrin receptor (TFRC), a positive regulator of ferroptosis, was upregulated by ART and DHA.