Mccartyquinlan4717

Although accumulating evidence has confirmed the potential biological functions of long non-coding RNAs (lncRNAs) as competitive endogenous RNAs (ceRNAs) in colorectal tumorigenesis and progression, few studies have focused on rectosigmoid junction cancer. In the present study, a comprehensive analysis was conducted to explore lncRNA-mediated ceRNA implications and their potential value for prognosis. lncRNA, microRNA (miR/miRNA) and mRNA expression profiles were downloaded from The Cancer Genome Atlas database. Subsequently, a lncRNA-miRNA-mRNA regulatory network was constructed to evaluate the functions of these differentially expressed genes on overall survival (OS) for rectosigmoid junction cancer. As a result, a rectosigmoid junction cancer-specific ceRNA network was successfully constructed with 7 differentially expressed (DE)lncRNAs, 16 DEmiRNAs and 71 DEmRNAs. Among the network, one DElncRNA (small nucleolar RNA host gene 20) and three mRNAs (sodium- and chloride-dependent taurine transporter, fibroblast growth factor 13 and tubulin polyglutamylase TTLL7) were significantly associated with OS (P less then 0.05). Additionally, two lncRNAs (KCNQ1OT1 and MIR17HG) interacted with most of the DEmiRNAs. Notably, two top-ranked miRNAs (hsa-miR-374a-5p and hsa-miR-374b-5p) associated networks were identified to be markedly associated with the pathogenesis. Furthermore, four DEmRNAs (caveolin-1, MET, filamin-A and AKT3) were enriched in the Kyoto Encylopedia of Gene and Genomes pathway analysis, as well as being included in the ceRNA network. In summary, the present results revealed that a specific lncRNA-miRNA-mRNA network was associated with rectosigmoid junction cancer, providing several molecules that may be used as novel prognostic biomarkers and therapeutic targets.Fusobacterium nucleatum (Fn) is considered a promoting factor in colorectal cancer (CRC); however, only a few studies have investigated therapies against Fn. L-fucose is a natural monosaccharide that has prebiotic potential. The present study aimed to investigate the effect of L-fucose on the carcinogenic properties of Fn. The HCT116 and SW480 colon cancer cell lines were treated with Fn and Fn+L-fucose (Fnf), respectively. The Cell Counting Kit-8 (CCK-8), colony formation, Transwell migration and invasion and wound healing assays were performed to assess the proliferative, migratory and invasive abilities of the cells, respectively. Western blot was performed to detect the protein levels of jak/stat3 pathway components and EMT. The results of the CCK-8, colony formation, Transwell and wound healing assays demonstrated that treatment with Fn significantly enhanced the proliferative, migratory and invasive abilities of HCT116 and SW480 colon cancer cells. Notably, these effects were significantly reversed following addition of L-fucose. Furthermore, L-fucose inhibited the carcinogenic properties of Fn to activate the stat3 pathway and epithelial-to-mesenchymal transition. Taken together, the results of the present study suggest that L-fucose ameliorates the carcinogenic properties of Fn in vitro, and thus may serve as a novel therapeutic target for flora-related colon cancer.The accurate evaluation of human epidermal growth factor receptor 2 (HER2) status is essential for the appropriate use of targeted therapies. An increased number of chromosome 17 centromere enumeration probe (CEP17) signals may underrate fluorescence in situ hybridization (FISH) outcomes, resulting in false-negative or a false-equivocal HER2 status assessment. The aim of the present study was to assess the frequency of CEP17 copy number increase (CNI), its effects on HER2 protein expression (and the subsequent effects on tumor cells), and the survival outcomes of patients with gastric cancer. Archival primary tumor samples from 244 patients that underwent gastric resection for adenocarcinoma were retrieved for both HER2 protein expression analysis (using immunochemistry) and HER2 gene amplification (using FISH). The associations between HER2 status, CEP17 CNI and multiple clinicopathological parameters (including survival outcome), were assessed. The relationship between CEP17 CNI and HER2 protein upregulation was also investigated. CEP17 CNI was detected in 17.2% of cases, and a strong association between CEP17 CNI and HER2 upregulation was revealed. The impact of CEP17 CNI on survival did not reach statistical significance. Consequently, CEP17 CNI was discovered to be strongly associated with HER2 upregulation in tumor cells, which may characterize a critical issue in HER2 testing. Therefore, the eligibility for HER2-targeted agents in CEP17 CNI-positive patients warrants further recognition.Small cell lung cancer (SCLC) is a subtype of lung cancer with a poor prognosis, with bone metastasis being one of the main causes of treatment failure. Therefore, investigating new biomarkers associated with bone metastasis may result in positive treatment outcomes. The present study detected the expression levels of annexin A1 (ANXA1) in the serum of 82 patients with SCLC using ELISA. ANXA1 expression in patients with SCLC with bone metastasis was significantly higher compared with that in patients without bone metastasis. Receiver operating characteristic analysis revealed that ANXA1 expression was significant in the diagnosis of bone metastasis in SCLC. ANXA1 was inhibited in SBC-5 cells and overexpressed in SBC-3 cells. Results revealed that ANXA1 was able to enhance SCLC cell proliferation, invasion, migration and bone adhesion in vitro. In vivo xenograft bone metastasis assays indicated that ANXA1 had the potential to promote the bone-metastasis ability of SCLC cells in NOD/SCID mice. Furthermore, ANXA1 increased parathyroid hormone-related protein secretion and enhanced Smad2 phosphorylation following TGF-β treatment in SCLC cells. Overall, ANXA1 may be involved in the pathogenesis of bone metastasis in SCLC and may be a potential biomarker for the diagnosis of SCLC.Anaesthetics have been implicated to influence cancer cells and progression. INF195 Similarly, crosstalk between cancer cells and stromal components within the microenvironment is also an important factor driving progression. Stromal cell-derived factor-1 (SDF-1) and hepatocyte growth factor (HGF) are key chemokines/cytokines produced by fibroblasts which have been established as influential factors in cancer progression. The present study explored the capacity of anaesthetics to influence the expression of these key molecules in fibroblasts. The anaesthetics rocuronium bromide (RB), vecuronium bromide (VB), suxamethonium chloride CRS (SCC), dexmedetomidine hydrochloride (DH) and lidocaine were used to treat MRC-5 fibroblasts over a range of concentrations. Following treatment, transcript expression of SDF-1 and HGF was quantified using quantitative PCR. Treatment of MRC-5 cells with RB brought about a reduction of SDF-1 expression which was found to be significant in the 45 µg/ml treatment group. Treatment with the other anaesthetics brought about some alterations in SDF-1 expression but these were not found to be statistically significant.