Mchughgates3795

Conclusion Our results suggest that for management of IBD patients, policymakers should address shifting the medical costs to biological agents, the higher cost of CD, and the impact of underlying factors on the distribution of these medical costs. ©2019 RIGLD.Aim The aim of this study was to determine gene expression levels of TNF-α, NOTCH1, and HES1 in patients with UC. Background Intestinal inflammation and epithelial injury are the leading actors of inflammatory bowel disease (IBD), causing an excessive expression of pro-inflammatory cytokines such as TNF-α. Also, target genes of NOTCH signaling are involved in the regulation of intestinal homeostasis. Previous studies have demonstrated that TNF-α increases in ulcerative colitis (UC) patients, but the relationship between TNF-α and NOTCH signaling pathway in UC etiopathology needs further study. Methods Twelve active UC patients and twelve healthy controls were enrolled in this study. RNA was extracted and the mRNA expression levels of TNF-α, NOTCH1, and HES1 were examined using real-time PCR analyses. Further, transcriptome data deposited in Gene Expression Omnibus (GEO) database were analyzed to detect the differential expression of TNF superfamily and NOTCH1 gene in IBD patients. Finally, the interaction of TNF-α and NOTCH signaling was obtained from The SIGnaling Network Open Resource 2.0 (SIGNOR 2.0) database. Results The transcription levels of TNF-α, NOTCH1, and HES1 genes were significantly elevated in UC patients compared with control (p less then 0.05). In addition, GEO results confirmed our expression results. SIGNOR analysis showed that TNF-α interacts with NOTCH signaling components. Conclusion Based on our data, we observed that NOTCH1 and HES1 in co-operation of TNF-α, may play an important role in pathogenesis of UC. The members of NOTCH signaling pathway can be ideal candidates to target the therapy of IBD. ©2019 RIGLD.Aim The aim of this study was to evaluate the effect of intestinal microbiota metabolites in colorectal cancer patients on HT29 cell line using MTT assay. Background Colorectal cancer is one of the most common malignant tumors. Human guts harbor abundant microbes that adjust many aspects of the host physiology. Increasing studies suggest that gut microbiota play a significant role in the incidence and expansion of CRC, as a result of virulence factors, bacterial metabolites, or inflammatory pathways. Methods In this cross-sectional study, 60 biopsy samples including 30 cancerous and 30 adjacent healthy tissues were collected from patients with CRC during 2017. Biopsy samples were first cultured on Thioglycollate broth medium for 24hr after which the microbiota metabolites were filtered and stored at -20 C° for further evaluation. HT29 cells were treated by microbiota metabolites at different times (3, 6, 12, 18h) and its viability was assessed by MTT assay. Results The cells treated with microbiota metabolites showed increased viability and proliferation in time-dependent analysis by MTT assay, but there was not significant differences between the two groups. Conclusion It seems that microbial metabolites are able to induce proliferation and increase cell viability and thus induce colorectal cancer. ©2019 RIGLD.Aim Identifying the critical genes that differentiate gall bladder cancer from a normal gall bladder and the related biological terms was the aim of this study. Background The molecular mechanism underlying gall bladder cancer (GBC) trigger and development still requires investigations. Potential therapeutic biomarkers can be identified through protein-protein interaction network prediction of proteome as a complementary study. Methods Here, a literature review of proteomics studies of gall bladder cancer from 2010 to 2019 was undertaken to screen differentially expressed proteins in this cancer. A network of 27 differentially expressed proteins (DEPs) via Cytoscape 3.7.1 and its plug-ins was constructed and analyzed. Results Ten proteins were introduced as hub-bottlenecks among which four were from DEPs. The gene ontology analysis also indicated that positive regulation of multi-organism process and regulation of response to biotic stimulus are the most disrupted biological processes of GBC considering their relationships with the DEPs. Conclusion ACTG, ALB, GGH, and DYNC1H1, and relative biological terms were introduced as drug targets and possible diagnostic biomarkers. ©2019 RIGLD.Aim This study set out to determine the effect of methylation on MALAT1 gene in primary colorectal lesions and tumors to gain further knowledge about the diagnostic and prognostic value of MALAT. Background Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is one of the long non-coding RNAs that plays an important role in invasion, cell proliferation, and metastasis of various cancers. However, there is insufficient information on the association between MALAT1 and the methylation process as well as its role in the development of colorectal cancer. Methods Methylation pattern of MALAT1 promoter was determined by Methylation-Specific Polymerase Chain Reaction (MSP) in 86 colorectal primary lesions, tumors, and normal specimens. MALAT1 methylation pattern was compared in tumor and polyp tissue. In order to obtain more accurate results, we investigated the association between MALAT1 promoter methylation pattern and clinicopathologic factors in patients. Results The results indicated that the MALAT1 promoter methylation pattern in the tumor tissue, primary lesion tissue, and normal was not significantly different (p=0.430). Comparison of the MALAT1 promoter methylation pattern between polyp types and tumor tissue groups was not significant either (p=0.437). Surprisingly, the methylation frequency of MALAT1 methylation was significantly higher in colon lesions than in their rectum lesion (p = 0.035). In addition, no significant hypermethylation of MALAT1 was observed between the other patients' clinicopathological data in both polyp 46/66 and tumor tissues 20/66. Conclusion This study dealt with determining the effect of methylation on MALAT1 gene in primary colorectal lesions and tumors to gain further knowledge about the diagnostic and prognostic value of MALAT. ©2019 RIGLD.Aim Given the high similarity of phenotypical and secretory properties of mesenchymal stem cells and fibroblasts, this study investigated the possibility of inducing EMT process by mesenchymal stem cells. Background Annually, more than 13% of deaths worldwide occur due to cancer. One of the main reasons for the high mortality rate is due to the metastasis of cancer stem cells. Induction of metastasis occurs during the EMT process, which can also be stimulated by fibroblast cells. Methods Mesenchymal stem cells (MSCs) were isolated and sub-cultured until passage 3 or 4. AGS cells were co-cultured with MSCs for 4 days. As the positive control group, AGS cells were treated with TGF-β (10ng/ml) for 48h. Finally, the mRNA expression level of Vimentin, β-catenin, Snail, and E-cadherin as the EMT pattern, were evaluated by RT-PCR technique. Results Our findings indicated that AGS cells' crosstalk with MSCs significantly upregulated fibroblast markers including Vimentin and Snail expression. However, no significant changes were identified for β-catenin gene expression. Additionally, AGS treatment with MSCs resulted in diminished E-cadherin in the targeted cells. Conclusion Based on the results, the AGS cells crosstalk with MSCs activates induction of epithelial mesenchymal transition, which is confirmed through the elevation of Vimentin and Snail expression and reduction of E-cadherin expression as a specific epithelial marker. However, it seems that MSc was not effective on Wnt/ β-catenin signal gastric cancer cell line. ©2019 RIGLD.Aim The main goal of this investigation was to provide an overview on H.pylori effect on gastric tissue via bioinformatics analysis of microarray-identified miRNAs and its target genes. Background MicroRNAs which control about 30 to 60% of gene expression in human body play a critical role in different cell growth stages. Expression modification of non-coding (NC) RNAs in H.pylori infections requires further investigations to provide better understanding of their roles in the body. Methods GSE54397, the microRNA microarray dataset, was analyzed by GEO2R, the online GEO database for detection of differentially expressed microRNAs and lastly the potential target genes as well as their associated pathways. Results A total of 244 miRNAs were detected as differentially expressed (p2) in non-cancerous tissue of gastric with H.pylori infection in comparison with tissues without H.pylori infection. The findings indicated that hub microRNAs and target genes of up-regulated network are KIF9, DCTN3, and CA5BP1 along with hsa-miR-519d, hsa-miR-573, hsa-miR-646, hsa-miR-92a-1, hsa-miR-186, and hsa-miR-892a, respectively. For the down-regulated network, genes of RABGAP1, HSPB11 and microRNAs of hsa-miR-620, hsa-miR-19b-2, hsa-miR-555, and hsa-let-7f-2 were hubs. Most of the up-regulated microRNAs are involved in gastric cancer development while there is no evidence for the down-regulated ones. Yet, all of the hub down-regulated miRNAs are reported to have associations with different kinds of cancer. Conclusion The introduced hub miRNAs and genes may serve as feasible markers in the mechanisms of H.pylori infection for different kinds of gastric diseases, in particular gastric cancer. However, their role requires further investigations. ©2019 RIGLD.Aim We used mixture cure mode to separately investigate the risk factors for long-term and short-term survival of colorectal cancer patients. Background Colorectal cancer (CRC) is the second most common cancer worldwide. In cancer studies, patients' survival is the most important indicator of patients' status. Classical methods in analyzing the survival data usually apply Cox proportional hazard regression. Methods The study was performed on 1121 patients diagnosed with colorectal cancer. Mixture cure model with Weibull distribution and logit link function was fitted to data. Results Odds of long-term survival for rectum cancer patients were lower than for colon cancer patients (OR=0.29(0.09, 0.9)). Also, patients with the advanced stage of the disease had lower odds of long-term survival compared to early-stage patients (OR=0.24(0.06, 0.86)).In the short-term, the hazard of death for people with normal BMI was lower than the underweight group (HR=0.4(0.21, 0.76)). The short-term hazard of death for rectum cancer was about half of the short-term hazard for colon cancer (HR=0.49(0.29, 0.81)). Further, people with moderately (HR=2.11(1.26, 3.55)) and poorly (HR=4.04(2.03, 8.03)) differentiated tumor grade had a higher short-term hazard of death compared to people with well-differentiated grade. Conclusion Predictive variables of colorectal cancer survival showed different effects in short- and long -terms. Site topography was a prognosis for both long-term and short-term survival; BMI and tumor grade were short-term predictors of survival while stage was a long-term predictor of survival. ©2019 RIGLD.Aim This study aimed to determine the link between Snail1 expression and CRC patients' survival as well as its significant association with EMAST status. Background Snail1 is an evolutionary preserved zinc-finger transcription protein which contributes to Epithelial-to-mesenchymal transition (EMT). EMT initiates invasion and proliferation in many tumors. Elevated microsatellite alteration at selected tetranucleotide repeats (EMAST) is a marker of poor prognosis in patients with colorectal cancer (CRC). We hypothesized that Snail1 overexpression is an important mediator of metastasis and decreased survival in CRCs that characteristically have EMAST phenotype. Methods Quantitative real-time polymerase chain reactions were carried out to analyze the expression levels of Snail1 in both normal and tumor specimens from a total of 122 paraffin-embedded tissues (FFPE) of CRC sample with known EMAST status. The correlation between Snail1 expression and clinicopathological characteristics, survival, and EMAST status were examined.