AIMTo provide an updated assessment of the safety and efficacy of enhanced recovery after surgery (ERAS) protocols in elective gastric cancer (GC) surgery.METHODSPubMed, Medline, EMBASE, World Health Organization International Trial Register, and Cochrane Library were searched up to June 2017 for all available randomized controlled trials (RCTs) comparing ERAS protocols and standard care (SC) in GC surgery. Thirteen RCTs, with a total of 1092 participants, were analyzed in this study, of whom 545 underwent ERAS protocols and 547 received SC treatment.RESULTSNo significant difference was observed between ERAS and control groups regarding total complications (P = 0.88), mortality (P = 0.50) and reoperation (P = 0.49). The incidence of pulmonary infection was significantly reduced (P = 0.03) following gastrectomy. However, the readmission rate after GC surgery nearly tripled under ERAS (P = 0.009). ERAS protocols significantly decreased the length of postoperative hospital stay (P < 0.00001) and medical costs (P < 0.00001), and accelerated bowel function recovery, as measured by earlier time to the first flatus (P = 0.0004) and the first defecation (P < 0.0001). Moreover, ERAS protocols were associated with a lower level of serum inflammatory response, higher serum albumin, and superior short-term quality of life (QOL).CONCLUSIONCollectively, ERAS results in accelerated convalescence, reduction of surgical stress and medical costs, improved nutritional status, and better QOL for GC patients. However, high-quality multicenter RCTs with large samples and long-term follow-up are needed to more precisely evaluate ERAS in radical gastrectomy.

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Background: The mortality rate for liver cancer is high worldwide. The etiology of liver cancer has altered with the high incidence rate of non-alcoholic fatty liver disease (NAFLD) although effective vaccination strategies have been developed. Therefore, it is important to discover new biomarkers for diagnosis and prognosis. Aquaporin 9 (AQP9) has been reported in some cancers, especially in liver cancer, although its role in this malignancy remains to be clarified. In this study, we conducted a bioinformatics analysis to clarify the function of AQP9 in liver cancer.Methods: Immunohistochemistry, real-time qPCR, western blot analysis were applied to detect AQP9 expression in tissue samples or cells. Online databases were used to analyze the correlation of AQP9 expression and clinical factors. LinkedOmics and gene set enrichment analysis (GSEA) were used to analyze the functional network of AQP9 in hepatocellular carcinoma (HCC). Four authoritative databases were used to predict the candidate microRNAs that bind to AQP9. Finally, we used the Tumor Immune Estimation Resource (TIMER) to assess the correlation of AQP9 and immune cell infiltration in HCC.Results: All analysis were revealed AQP9 is significantly decreased in HCC tissues and cells. AQP9 was negatively correlated with different tumor stage, grade, and weight, as well as lymph node metastasis, sex, and histological subtypes. AQP9 can be used to predict the prognosis of HCC patients. GSEA revealed that AQP9 was significantly involved in most significant hallmark pathways. LinkedOmics was used to analyze the relationship of AQP9 with Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Mechanistically, mir-23a-3p and mir-330-3p may downregulate AQP9 expression in HCC. AQP9 was found to be specifically correlated with immune cell infiltration and play a major role in the liver cancer microenvironment.Conclusions: In this study, we found that AQP9 was significantly decreased in HCC, with low AQP9 levels indicating a poor outcome. GSEA analysis and LinkedOmics revealed that AQP9 was significantly involved in the most significant hallmarks pathways. Mir-23a-3p and mir-330-3p may inhibit AQP9 expression in HCC. Our results also suggest that AQP9 is important in tumor immunity in the liver cancer.

Background: Liver cancer is one of the major causes of cancer death worldwide, incurring high mortality and a significant financial burden on the healthcare system. Abnormal RNA-binding proteins (RBPs) have been found to be associated with carcinogenesis in liver cancer. Among these, RNA-binding motif protein 12 (RBM12) is located in the exon junction complex (EJC). The goal of this study was to determine what role RBM12 plays in hepatocellular carcinoma (HCC) from a biological perspective. Methods:The Tumor IMmune Estimation Resource (TIMER) and the Human Protein Atlas database were used to examine the expression level of RBM12, with the UALCAN and Gene Expression Profiling Interactive Analysis (GEPIA) databases used to investigate the relationship between RBM12 and other noteworthy clinical features. RBM12 expression in cells and tissue samples was detected using quantitative real-time polymerase chain reaction (qRT-PCR) and western blot analysis. The functional network of RBM12 in HCC was studied using LinkedOmics and gene set enrichment analysis (GSEA), while the effects of hypomethylation on the expression of RBM12 in HCC was investigated using methylation databases. Finally, we used TIMER and CIBERSORT to investigate the relationship between immune cell infiltration and RBM12 in HCC.Results: RBM12 is highly elevated in HCC tissues and cells, and it can be used to predict the prognosis of patients with HCC. Analysis with LinkedOmics and GSEA revealed RBM12 to be closely linked with tumor progression. Furthermore, hypomethylation was linked to an increase in RBM12 expression in HCC, while RBM12 was associated with immune cell infiltration.Conclusions: This study shows that an elevated level of RBM12 in HCC indicates a poor patient prognosis. Furthermore, according to LinkedOmics and GSEA analyses, RBM12 was implicated in the most important hallmark pathways. Our findings suggest that RBM12 overexpression is caused by hypomethylation and that RBM12 plays a key role in liver cancer tumor immunity.

Background: Persistent Helicobacter pylori (H. pylori) infection leads to various gastric diseases. Multiple studies have demonstrated that aryl hydrocarbon receptor (AHR) plays roles in the antibacterial response and aryl hydrocarbon receptor repressor (AHRR) is downregulated in stomach cancer. However, the role of AHR or AHRR in H. pylori-related gastric diseases remains unclear.Aims: To investigate whether AHR or AHRR is involved in H. pylori-related gastric diseases.Methods: Patients with gastritis or gastric adenocarcinoma were enrolled randomly, and gastric tissue specimens were diagnosed pathologically. AHR, AHRR, and H. pylori infection status in tissues were detected by immunohistochemistry. Human gastric cells were cocultured with H. pylori. siRNAs were used to silence AHR or AHRR, and a C57bl/6 mouse model colonized by H. pylori was established. Protein expression was determined by western blotting analysis, and TNF, IL-8 and IL-1β in cell supernatants were measured by ELISA.Results: AHR and AHRR were expressed in gastritis tissues and gastric cancer tissues without H. pylori infection, and principally located in the cytoplasm and nucleus. AHR expression was significantly correlated with AHRR expression in gastric tissues without H. pylori infection (P=0.008). However, their expressions were negatively correlated with H. pylori infection status. H. pylori coculture inhibited AHR and AHRR expression in stomach mucosa in vitro and in vivo. Gastric cells produced more TNF, IL-8 and IL-1β when AHR or AHRR was silenced.Conclusions: This preliminary study indicates that AHR and AHRR may be involved in H. pylori-related gastric pathogenesis, and helps toward understanding of inflammation-initiated carcinogenesis of gastric cancer.