Background:Human leukocyte antigen-E (HLA-E)is a non-classical major histocompatibility complex (MHC) class I antigens which expressed on extra villous cytotrophoblast, which interacts with NKG2A, is an inhibitory receptor on natural killer (NK) cells and leading to down regulation of immune response in the maternal-fetal interface and provides maternal immune tolerance of the fetus.Objective:This study was designated to investigate the gene frequencies of E0101 and E0103 in HLA-E gene in Iranian women with recurrent spontaneous abortion (RSA). Materials and Methods:Amplification Refractory Mutation System (ARMS-PCR) technique was carried out to detect polymorphism in exon 3 of the HLA-E gene in women with RSA and controls (n=200). Differences between groups were analyzed by SPSS19 software using 2 test.Results:There was no significant difference in the allele frequencies of the HLA-E polymorphism between RSA and fertile controls but HLA-E 0101/0103 heterozygous genotype was found to be significantly higher in RSA group (p=0.006, OR=1.73), so this genotype might confer susceptibility to RSA.Conclusion: Our results suggest that HLA-E 0101/0103 heterozygous genotype leads to increase of RSA risk. It seems that by genotyping of HLA-E polymorphism, we can predict the risk of RSA in infertile women.
Background: The most malignant form of infiltrating astrocytoma, glioblastoma multiforme (GBM), is one of the most aggressive human cancers. Foretinib diminished GBM cell invasion by downregulating the expression of matrix metalloproteinase 2 (MMP2).
Aim: The study aimed to examine the anti-tumor activity of foretinib and to test its effect on MMP2 expression in T98 cells.
Materials and Methods: T98 cells were used as an experimental model of glioblastoma. The effect of foretinib on the expression of MMP2 was evaluated using quantitative real-time polymerase chain reaction. Thereafter, the effect of foretinib on the enzyme levels of MMP was examined by zymography. Statistical analyses were performed with GraphPad Prism software.
Results: A reduction in the expression of MMP2 was observed with an increase in the concentration of foretinib.
Conclusion: Foretinib treatment leads to downregulation of MMP-2 and has a positive effect on T98 cells. We believe that foretinib can be subjected to further clinical investigation to develop a treatment for GBM.
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