BackgroundGastrointestinal cancers (GICs) mainly including esophageal, gastric and colorectal cancer, are the most common cause of cancer-related death and lead into high mortality worldwide. We performed this systematic review and meta-analysis to elucidate relationship between multiple microRNAs (miRs) expression and survival of GIC patients.MethodsWe searched a wide range of database. Fixed-effects and random-effects models were used to calculate the pooled hazard ratio values of overall survival and disease free survival. In addition, funnel plots were used to qualitatively analyze the publication bias and verified by Begg's test while it seems asymmetry.Results60 studies involving a total of 6225 patients (1271 with esophageal cancer, 3467 with gastric cancer and 1517 with colorectal cancer) were included in our meta-analysis. The pooled hazard ratio values of overall survival related to different miRs expression in esophageal, gastric, colorectal and gastrointestinal cancer were 2.10 (1.78-2.49), 2.02 (1.83-2.23), 2.54 (2.14-3.02) and 2.15 (1.99-2.31), respectively. We have identified a total of 59 miRs including 23 significantly up-regulated expression miRs (miR-214, miR-17, miR-20a, miR-200c, miR-107, miR-27a, etc.) and 36 significantly down-regulated expression miRs (miR-433, let-7g, miR-125a-5p, miR-760, miR-206, miR-26a, miR-200b, miR-185, etc.) correlated with poor prognosis in GIC patients. Moreover, 35 of them revealed mechanisms.ConclusionOverall, specific miRs are significantly associated with the prognosis of GIC patients and potentially eligible for the prediction of patients survival. It also provides a potential value for clinical decision-making development and may serve as a promising miR-based target therapy waiting for further elucidation.
Gastrointestinal cancers (GICs) are a huge threat to human health, which mainly include esophageal, gastric, and colorectal cancers. The purpose of this study was to clarify the prognostic value of long noncoding RNAs (lncRNAs) in GICs. A total of 111 articles were included, and 13103 patients (3123 with esophageal cancer, 4972 with gastric cancer, and 5008 with colorectal cancer) were enrolled in this study. The pooled hazard ratio (HR) values and corresponding 95% confidence interval (95% CI) of overall survival (OS) related to different lncRNA expressions in esophageal, gastric, colorectal, and gastrointestinal cancer patients were 1.92 (1.70–2.16), 1.96 (1.77–2.16), 2.10 (1.87–2.36), and 2.00 (1.87–2.13), respectively. We have identified 74 lncRNAs which were associated closely with poor prognosis of GIC patients, including 58 significantly upregulated lncRNA expression and 16 significantly downregulated lncRNA expression. In addition, 47 of the included studies revealed relative mechanisms and 12 of them investigated the correlation between lncRNAs and microRNAs. Taken together, this meta-analysis supports that specific lncRNAs are significantly related to the prognosis of GIC patients and may serve as novel markers for predicting the prognosis of GIC patients. Furthermore, lncRNAs may have a promising contribution to lncRNA-based targeted therapy and clinical decision-making in the future.
Hepatocellular carcinoma (HCC) is a common malignancy with a poor prognosis worldwide. However, the pathogenesis of HCC remains poorly understood. In this study, we found that NOL12 was significantly overexpressed in independent HCC datasets from TCGA database. We confirmed that the expression level of NOL12 was upregulated in human HCC tissues and cell lines by RT-qPCR. High expression of NOL12 is associated with worse reduced overall survival (OS), high pathological grade, node metastasis, and advanced clinical stage in patients with HCC. Moreover, knockdown of NOL12 dramatically inhibits the proliferation and metastasis of HCC cells in vitro and in vivo. CIBERSORTx analysis revealed that twelve types of tumor-infiltrating immune cells (TICs) are correlated with NOL12 expression. The risk signature based on 8 NOL12-related genes is an independent prognostic factor for patients with HCC. The OS rate of patients in the low-risk score group was better than that in the high-risk score group. In addition, the total tumor mutation burden (TMB) in the high-risk score group increased significantly, and the risk scores could be used as an alternative indicator of immune checkpoint inhibitor (ICI) response. In conclusion, our findings indicated that NOL12 might be involved in the progression of HCC and can be used as a potential therapeutic target. Moreover, the NOL12-related risk signature may have predictive relevance with regard to ICI therapy.
Background. Immunotherapy is an important treatment modality for gastric cancer, therefore, it is crucial to understand the regulators of the tumor microenvironment in gastric cancer. Numerous studies have shown that noncoding RNAs have a critical status in the tumor progression, and the influence of competing endogenous RNA (ceRNA) networks on gastric adenocarcinoma has been widely discussed over the years, but the connection between ceRNA networks and the immune microenvironment of cancer is unclear. This study was aimed at exploring how ceRNA networks influence the prognosis of patients with gastric cancer by modulating the tumor microenvironment. Methods. The Gene Expression Omnibus was analyzed to obtain differential expression matrixes of the noncoding RNAs (circular RNAs (circRNAs), microRNAs (miRNAs)), and mRNAs. The Circular RNA Interactome web tool and TargetScan were applied to determine the miRNA binding sites of the circRNAs and miRNA target genes. The Cancer Genome Atlas provided prognostic genes for gastric cancer, and Cytoscape created the ceRNA networks. Real-time quantitative reverse transcription polymerase chain reaction and western blot assay were adopted to find out how the ceRNA network regulates the expression of the hub gene. Additionally, the TISIDB and TIMER databases were used to assess the link between the hub gene and immunotherapy, with TISIDB providing the immune genes that are coexpressed with the hub gene. Furthermore, the immune-gene signature was constructed by using Cox regression analysis. Moreover, the nomogram, which could predict the prognostic role of gastric cancer patients was created on the basis of the immune-gene signature. Results. In gastric cancer, the circ-0007707/miR-429/PDGFD pathway had a differential expression. The results demonstrated that the pathway could regulate the progression and immune microenvironment of gastric cancer by modulating the immune-gene signature, which included two immune genes (TAB1 and CXCR4). Moreover, the low-risk group patients had better survival. Conclusion. The circ-0007707/miR-429/PDGFD pathway may play a regulatory role in the progression and prognosis of gastric cancer by interfering with the tumor microenvironment, and the PDGFD-related immune-gene signature could be considered a moderator of prognostic factor for gastric cancer and to guide immunotherapy programs.
Background: The clinical significance of Raman spectroscopy (RS) in colorectal cancer (CRC) patients still remains underestimated. We performed this meta-analysis to elucidate the diagnostic value in CRC patients. Methods: We systematically searched electronic databases for published articles. Fixed effect model and random effect model were used to calculate the pooled sensitivity, specificity, diagnostic accuracy, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR) and positive posttest probability (PPP) of CRC. Meta-regression and subgroup analysis were conducted to assess potential source of heterogeneity. We also used Egger linear regression tests to assess risk of publication bias. Results: Thirteen studies had been included (679 patients: 186 with premalignant lesions and 493 with malignant lesions). The pooled sensitivity, specificity, diagnostic accuracy, PLR, NLR, DOR and PPP for CRC screening using RS were 0.94 (0.92–0.96), 0.94 (0.88–0.97), 0.96 (0.94–0.98), 16.44 (7.80–34.63), 0.062 (0.043–0.090), 263.65 (99.03–701.96) and 86%, respectively. Conclusion: RS is a potentially useful tool for future CRC screening. It also offers potentially early detection for CRC patients.
Background: Cancer stem cells (CSCs) are the main cause of resistance to anti-cancer drug therapy and distant metastasis of tumors, including gastric cancer. The metabolism of CSCs is an important factor in the maintenance of its stemness. This study is intended to explore the role of oxidative phosphorylation in gastric CSCs. Methods: EpCAM+CD44+ gastric CSCs were sorted from the SGC-7901 cell line. The oxidative phosphorylation and glycolysis were determined by Seahorse experiment, and the oxygen consumption of cells was determined by Clark’s oxygen electrodes. Gene expression and protein levels of mitochondrial proteins belonging to five respiratory chain complexes were checked. Phenformin and siRNA-NDUFB8 were used to inhibit respiratory chain complex I to explore the biological effect of enhanced oxidation phosphorylation in gastric CSCs. Cell migration capacity, proliferation ability, and vascular endothelial growth factor (VEGF) levels were also evaluated. Results: Compared with control cells, the oxidation phosphorylation in mitochondria increased in EpCAM+CD44+ gastric CSCs, although the respiration level remained the same, and no significant changes were observed in glycolysis. Moreover, mRNA and protein expression levels of NDUFB8 in complex I were significantly increased. However, oxidative phosphorylation decreased in EpCAM+CD44+ cells after the treatment of phenformin and siRNA-NDUFB8 compared to the untreated cells. siRNA for NDFUB8 and phenformin inhibition also decreased the ability of cell migration, cell proliferation, as well as the VEGF secretion of gastric CSCs. Conclusion: These results suggest that the increased oxidative phosphorylation was related to respiratory chain complex I and NDUFB8 in gastric CSCs.
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