فهرست مطالب farhad babaie

Snail-1 is a transcription factor, which takes part in EMT, a process related to the emergence of invasion and cancer progression. The purpose of this study was to evaluate the effect of Snail-1 silencing on the human esophageal squamous cell carcinoma cell line, namely TE-8, in vitro. In this study, transfection of Snail-1 specific siRNA was conducted into TE-8 cells. The relative mRNA expression levels of Snail-1, Vimentin, CXCR4 and MMP-9 and transcription levels of miR-34a and let-7a were investigated by quantitative Real-time PCR. Western blotting was carried out to evaluate the Snail-1 protein level. Migration assay of TE-8 cells was also performed following the presence or absence of Snail-1 specific siRNA. MTT and TUNEL assays were performed to evaluate cell viability after Snail-1 silencing. It was found that treatment of cancer cells with the Snail-specific siRNA effectively downregulated the expression of Snail-1 in both mRNA and protein levels, and vimentin, CXCR4, and MMP-9 in mRNA level. However, it elevated the transcript levels of miR-34a and let-7a expressions. Furthermore, transfection of cancer cells with the Snail-specific siRNA significantly induced apoptosis in TE8 cells. Moreover, suppression of Snail-1 led to diminished cell migration. It seems that Snail-specific siRNA can significantly interrupt esophageal cancer cell migration and reduce metastatic-related factors and induce miR-34a and let-7a in vitro. The bottom line is that therapeutic approaches via targeting Snail-1 can be used for ESCC treatment, suggesting that other possible target molecules for ESCC therapy require to be explored.

Ankylosing spondylitis (AS), an autoinflammatory disease, has been associated with impaired Endoplasmic reticulum aminopeptidase (ERAP) 1 activity, which is involved in priming antigenic peptides. The purpose of this study was to evaluate if the genetic variant of ERAP1 gene could impress the inflammation status of the AS patients. For genotyping, 140 AS cases and 140 healthy controls were enrolled. After isolation of peripheral blood mononuclear cells (PBMCs) and DNA extraction, all the subjects were genotyped for rs27044 polymorphism using SSP-PCR assay. Total RNA of PBMCs was isolated, cDNA was synthesized, and quantitative analyses of mRNA expression of cytokines were performed via Real-time PCR using the SYBR Green Gene Expression MasterMix. To measure the concentration of cytokines in serum of subjects, Enzyme-linked immunosorbent assay (ELISA) was used. It was observed that the G allele of rs27044 polymorphism was significantly prevalent in AS patients. Moreover, the GG genotype and the GG+GC dominant model had significantly different distribution between study groups. There was a significant overexpression of mRNAs of IL-17A, IL-6, IL-33, TNF-α, and IFN-γ, while IL-10 was significantly downregulated in AS patients. The ELISA results were in line with that of the gene expression analysis. No significant differences in mRNA expression and concentration of cytokine were identified among AS patients with three genotypes for rs27044 SNP. This study replicated the association of polymorphisms in ERAP1 gene with the risk of AS in a population from Iranian. However, it did not directly determine the inflammatory profile of the AS patients.

Bakground: Multiple sclerosis (MS) is a CD4+ T cell-mediated autoimmune diseaseaffecting the central nervous system (CNS). It was previously believed that Th1 cells werepathogenic T cells in experimental autoimmune encephalomyelitis (EAE). However, thefunctional role of Th1 cells in EAE has been reconsidered upon the discovery of IL-17-producing T cells which are consider as dominant effectors for inducing autoimmune tissueinflammation. The objective of this study was to assess the role of IL-17A andIL-17F in MS pathogenesis. We evaluated mRNA expression of IL-17A andIL-17F in thirty-five Iranian patients with relapsing–remitting MS (RRMS) and twenty-fivehealthy controls by Quantitative Real Time PCR. The results of this study showed a twenty-fold increase in the expression of IL-17A mRNA in MS patients compared to the control group (p < 0.0001). IL-17F mRNA expression in MS patients was thirty three-times greater than control group (p = 0.0008). IL-17A mRNA expression in periphery was positively correlated with expression of IL-17F transcripts in MS patients and controls (p < 0.01 and p < 0.05, respectively). These results indicate the critical role of Th17- mediated cytokines in development of MS which classically has been considered as a Th1-mediated disorder. The results of this study showed, for the first time, the importance of IL-17F in MS immunopathogenesis.