Fibronectin 1 (FN1) is involved in the occurrence and development of various tumors and is upregulated in multiple cancer types. FN1 has been demonstrated to promote cell proliferation and migration in gastric cancer cell lines. However, the relationship between the expression of FN1 and clinicopathological factors and prognosis is not clear in gastric cancer (GC). The aim of the present study was to investigate the association between FN1 expression and clinicopathology and prognosis of gastric cancer. In this study, 17 publicly available GC cohorts (n=2,376) with gene expression data from the Gene Expression Omnibus (GEO), The Cancer Genome Atlas (TCGA) and Oncomine databases were tested. In addition, FN1 protein expression was validated by immunohistochemistry in a separate cohort (n=190). The meta-analysis results demonstrated an increase in FN1 expression at the protein and mRNA level in GC tissues, and the FN1 gene was highly expressed at the mRNA level in the advanced T stage (T2 + T3 + T4) group compared with that in the early T stage (T1) group. In addition, the expression of epithelial FN1 at the protein level was positively correlated with tumor size. FN1 expression at the protein and mRNA level was a predictor of poor prognosis following radical resection of GC. In conclusion, the expression of FN1 in GC tissues is upregulated compared with adjacent normal tissues, and it is a potential biomarker of poor prognosis in patients with GC.

Bradykinin (BK) has been reported to be involved in the progression of many types of cancer. In the present study, we investigated a possible role of BK in colorectal cancer cell invasion and migration. Invasion and migration assays showed that BK treatment promoted the invasion and migration of colorectal cancer cells. Further experiments showed that BK treatment stimulated ERK1/2 activation and IL-6 production. Two bradykinin receptors, bradykinin B1 receptor (B1R) and bradykinin B2 receptor (B2R), were significantly expressed in all the tested colorectal cancer cells. Repression of B2R, but not B1R, attenuated the BK-mediated invasion and migration, and inhibited ERK1/2 activation and IL-6 production. Moreover, blocking of the ERK pathway decreased the BK-mediated IL-6 production. In addition, IL-6 repression suppressed the effects of BK on colorectal cancer cell invasion and migration. Taken together, the present study demonstrated that BK increases IL-6 production via B2R and the ERK pathway, thereby contributing to the invasion and migration of colorectal cancer cells. Thus, our findings may provide benefits for the treatment of colorectal cancer.

MicroRNAs (miRNAs) play an important role in carcinogenesis. miR-218 is one of the most known miRNAs and has been demonstrated to inhibit progression in gastric cancer. However, the underlying molecular mechanism is not established. In this study, qRT-PCR and Western blot indicated that miR-218 was downregulated in gastric cancer cell lines SGC7901 and BGC823 compared to that in normal gastric epithelial cell line GES-1. MTT and wound scratch assays suggested that overexpression of miR-218 markedly suppressed cell proliferation, migration, and EMT of gastric cancer cells. Furthermore, we proved that WASF3 was a direct target of miR-218 by luciferase reporter assay, and restoration of WASF3 expression impairs miR-218-induced inhibition of proliferation, migration, and EMT in gastric cancer cells SGC7901. In summary, our results demonstrated that miR-218 functions as one of the tumor-suppressive miRNAs and inhibits gastric cancer tumorigenesis by targeting WASF3. miR-218 may serve as a potential therapeutic target for the treatment of gastric cancer.

Intensive glycemic control in diabetic patients receiving enteral nutrition after gastrectomy was associated with a lower surgical site infection rate but a higher hypoglycemia rate.

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Abstract. Diallyl disulfide (DADS) exerts anticarcinogenic activity in various types of cancer. However, the mechanism underlying its anticarcinogenic activity remains to be elucidated.

BackgroundNumerous pathological processes that affect liver function in patients with liver failure have been identified. Among them, hyperammonia is one of the most common phenomena.The purpose of this study was to determine whether hyperammonia could induced specific liver injury.MethodsHyperammonemic cells were established using NH4Cl. The cells were assessed by MTT, ELISA, and flow cytometric analyses. The expression levels of selected genes and proteins were confirmed by quantitative RT-PCR and western blot analyses.ResultsThe effects of 20 mM NH4Cl pretreatment on the cell proliferation and apoptosis of primary hepatocytes and other cells were performed by MTT assays and flow cytometric analyses. Significant increasing in cytotoxicity and apoptosis were only observed in hepatocytes. The cell damage was reduced after adding BAPTA-AM but unchanged after adding EGTA. The expression levels of caspase-3, cytochrome C, calmodulin, and inducible nitric oxide synthase were increased and that of bcl-2 was reduced. The Na+-K+-ATPase activities in hyperammonia liver cells was no signiaficant difference compaired with the control group, but was decreased in astrocytes. NH4Cl pretreatment of primary hepatocytes promoted the activation of mitochondrial permeability transition pores and the mitochondria swelled irregularly.ConclusionsHyperammonia induces specific liver injury through an intrinsic Ca2+-independent apoptosis pathway.

Background: Aberrant transcript alternative splicing is an important regulatory process closely connected with oncogenesis. Purpose: The objective of this study was to determine the phenotype and function of a novel long noncoding RNA (lncRNA) LINC00477 in gastric cancer. Patients and methods: The gastric cancer samples of 140 from Oncomine database and 17 from our own hospital, as well as three gastric cancer cell lines MKN-45, AGS and KATO III were used in this study. The expression of the spliced isoforms of LINC00477 were tested. The tumor effects of LINC00477 on gastric cancer were investigated in vitro and in vivo. The mechanism of LINC00477 interacted with aconitase 1 (ACO1) was further examined by RIP and pull down assay. Results: The overall expression of LINC00477 was reduced in gastric cancers compared to normal gastric tissues. The isoform 1 of LINC00477 was down-regulated while the isoform 2 was up-regulated in gastric cancer cells. The opposite role of isoforms 1 and 2 in the proliferation and migration of cancer cells in vitro and in vivo was observed. Furthermore, isoform 1 of LINC00477 was determined to interact with ACO1 and suppress the conversion ability from citrate to isocitrate by ACO1. Conclusion: we presented the important roles of the spliced isoforms of long noncoding RNA, LINC00477 in gastric carcinogenesis.