Comparison of the diagnostic efficacy of blue laser imaging with narrow band imaging for gastric cancer and precancerous lesions: a meta-analysis.

BACKGROUND AND AIMS: novel endoscopic techniques including narrowband imaging (NBI) and blue laser imaging (BLI) have led to the improved detection of early stage gastric cancer and precancerous lesions. However, these techniques are not generally thought to be equivalent at present and BLI is generally considered as superior to NBI. Therefore, this comprehensive meta-analysis aimed to definitively compare the diagnostic efficacy of NBI and BLI for the diagnosis of gastric cancer and precancerous lesions. METHODS: relevant articles were identified via searches of the PubMed, Web of Science, Embase and Cochrane Library databases from their inception until October 2019. In total, 28 relevant studies were identified and incorporated into the meta-analysis. RevMan5.3 was used to assess the relative diagnostic efficacy of these two imaging modalities in these studies. The threshold was assessed using Meta-DiSc 1.4 and STATA 14.0 for bivariate regression modeling of pooled studies. RESULTS: the pooled sensitivity of BLI for gastric cancer was 0.89 (0.80, 0.95) and the specificity was 0.92 (0.76, 0.98). The pooled sensitivity of NBI for gastric cancer was 0.83 (0.75, 0.89) and the specificity was 0.95 (0.91, 0.97). The pooled sensitivity of BLI for precancerous lesions was 0.81 (0.71, 0.87) and the specificity was 0.90 (0.80, 0.96). The pooled sensitivity of NBI for precancerous lesions was 0.80 (0.75, 0.85) and the specificity was 0.88 (0.77, 0.94). CONCLUSIONS: this study showed that both BLI and NBI have a very high diagnostic efficacy for the detection of gastric cancer and precancerous lesions, the sensitivity and specificity of these two approaches were similar.

Exosomal miR-552-5p promotes tumorigenesis and disease progression via the PTEN/TOB1 axis in gastric cancer.

Purpose Gastric cancer (GC) is associated with rapid disease progression and poor patient prognosis, highlighting the pressing need for new biomarkers to facilitate disease management. Exosomes are released by all cells and are ubiquitous in body fluids, thus giving them great potential as diagnostic biomarkers and therapeutic targets. MicroRNAs (miRNAs) can be transported by exosomes, and are a common target for regulation in cancer. Methods Our screen of miRNAs in the Gene Expression Omnibus and The Cancer Genome Atlas databases identified miR-552-5p as the most overexpressed miRNA in GC, and we investigated its function and mechanism of action. Results We detected high expression of miR-552-5p in GC tissues, plasma samples and cell lines. We found that miR-552-5p binds directly to the 3'-untranslated region of PTEN, and the resulting downregulation of PTEN in turn downregulates the tumor suppressor TOB1. Furthermore, experiments in cell culture and mice showed that miR-552-5p in exosomes is internalized by recipient cells, where it enhances proliferation, migration and the epithelial-mesenchymal transition, while suppressing the caspase-3 apoptotic pathway. These effects were reversed by inhibiting miR-552-5p. Conclusion GC-derived exosomal miR-552-5p facilitates tumorigenesis by interfering with the PTEN/TOB1 axis, providing new potential therapeutic targets.

MiR-199b-5p Promotes Gastric Cancer Progression by Regulating HHIP Expression.

OBJECTIVES: Gastric cancer (GC) is one of the most common malignant tumors. More and more evidences support the role of microRNAs (miRNAs) in tumor progression. However, the role of miRNAs in human GC remains largely unknown. METHODS: Based on the published gastric cancer expression profile data, combined with bioinformatics analysis, potential miRNAs in the process of GC were screened. The expression of miR-199b-5p in GC cells and patients' plasma was detected by RT-PCR. The effects of miR-199b-5p on GC in vitro were detected by EdU proliferation assay, colony formation assay, Transwell assay and wound healing assay. Western blot was used to detect epithelial-mesenchymal transition (EMT) related proteins. The subcutaneous tumorigenesis model and metastatic tumor model of mice were used to study its effect in vivo. Bioinformatics and Dual luciferase reporter assay were used to verify the effect of miR-199b-5p and its target gene. RESULTS: Through bioinformatics analysis, we screened a novel miRNA miR-199b-5p that was significantly up-regulated in GC tissue and associated with poor prognosis of GC patients. RT-PCR results showed that its expression was also up-regulated in GC cell lines and patients' plasma. MiR-199b-5p can significantly promote GC cell proliferation and migration in vitro and in vivo. Western blot showed that miR-199b-5p could promote the EMT process of GC. HHIP has been proved to be a target of miR-199b-5p, and the recovery of HHIP can weaken the effect of miR-199b-5p. CONCLUSION: MiR-199b-5p may play an oncogene role in GC by targeting HHIP, suggesting that miR-199b-5p may be a potential therapeutic target for GC.

Survival-Related lncRNA Landscape Analysis Identifies LINC01614 as an Oncogenic lncRNA in Gastric Cancer.

Background: Long non-coding RNAs (lncRNAs) reportedly play important roles in biomarker and tumorigenesis of gastric cancer (GC). This study aimed to determine the potential application of prognostic lncRNA signature and identified the role of LINC01614 in carcinogenesis in GC. Material and Methods: Data accessed from the Cancer Genome Atlas database was used to construct a lncRNA signature. Joint effect analysis of the signature and clinical parameters was performed to verify the clinical value of the signature. Co-expression analysis was conducted for prognostic lncRNAs and protein-coding genes. Moreover, the relative expression of LINC01614 was validated in GC tissues and cell lines. In vitro and in vivo experiments were conducted to analyze the biological functions of the newly identified gene in GC cells. Results: A seven-lncRNA (LINC01614, LINC01537, LINC01210, OVAAL, LINC01446, CYMP-AS1, and SCAT8) signature was identified as a promising prognostic signature in GC. Results indicated that the seven-lncRNA was involved in tumorigenesis and progression pathways. LINC01614 expression was identified and found to be upregulated in GC tissues and cells. The study findings revealed that LINC01614 promoted cell proliferation, migration, invasion, and epithelial-mesenchymal transition. Knockdown of LINC01614 arrested cell cycle distribution at the G2/M phase. Further, LINC01614 also promoted tumor growth in vivo. Conclusion: We developed an independent seven-lncRNA biomarker for prognostic prediction and identified LINC01614 as an oncogenic lncRNA in GC.

ICAM1 Regulates the Development of Gastric Cancer and May Be a Potential Biomarker for the Early Diagnosis and Prognosis of Gastric Cancer.

BACKGROUND: Gastric cancer (GC) is among the most common forms of cancer affecting the digestive system. This study sought to identify hub genes regulating early GC (EGC) in order to explore their potential for early diagnosis and prognosis of patients. METHODS: We utilized a publically available dataset from the Gene Expression Omnibus database (GSE55696). Differences between EGC and LGIN with respect to gene expression were compared using the limma software. Identified differentially expressed genes (DEGs) were subjected to gene ontology (GO) and pathway enrichment analyses with the DAVID application, and the STRING website and Cytoscape software were used to construct a protein-protein interaction (PPI) network incorporating these DEGs. This network was in turn used to identify hub genes among selected DEGs, which were analyzed with the Kaplan-Meier Plotter database. In addition, Western blotting, qRT-PCR, immunohistochemistry, and UALCAN were all employed to validate the relationship between the expression of these genes and GC patient prognosis. RESULTS: A total of 482 DEGs were identified, with GO analyses indicating an increase in the expression of genes linked with the development of cancer. Pathway analyses also indicated that these genes play a role in certain cancer-related pathways. The PPI network highlighted four potential hub genes, of which only ICAM1 was linked to a poor GC patient prognosis. This link between ICAM1 and GC patient outcomes was confirmed via UALCAN, Western blotting, immunohistochemistry, and qRT-PCR. CONCLUSION: ICAM1 may therefore modulate tumor progression in GC, thus potentially representing a valuable prognostic and diagnostic biomarker of EGC.