ABSTRACT
Aim: In present study we have elucidated the role of 2758 A>G [rs696], in the recognition site of miR449a in the 3' UTR of NFKB inhibitor alpha [NFKBIA] gene, in development of sporadic colorectal cancer
Background: Colorectal cancer [CRC] is rated as second cause of cancer death. Genetic determinants are considered as driving forces in development of sporadic CRC. Single nucleotide polymorphisms [SNPs], are attributed as the main genetic factor in cancers susceptibility. MicroRNAs, are key players in post-translational gene regulation by binding to their specific recognition sequences located at 3' untranslated region [UTR] of mRNAs
Methods: A case.control study using 143 CRC patients and 137 noncancerous counterparts were undertaken in order to determine rs696 genotypes using polymerase chain reaction. restriction fragment length polymorphism [PCR.RFLP] method
Results: There was a significant difference for the genotype frequencies of rs696 between patients and controls. The frequencies of GG, AG, AA genotypes in the control group were 38.7, 45.3, and 16.1 %, respectively, and the genotype frequencies in case group were 19.6, 40.6, and 39.9 %, respectively
Conclusion: Our results suggest significant correlation between rs696 polymorphism and colorectal cancer risk
ABSTRACT
Escherichia coli [E.coli] O157:H7 is one of the most important pathogenic causes of hemorrhagic colitis in humans. Cattle are the main reservoirs of this bacteria and vaccination is a key mechanism for its control. The intimin, translocated intimin receptor [tir], and EspA proteins are virulence factors expressed by the LEE locus of enterohemorrhagic E. coli. EspA protein is a member of the type III secretion system [TTSS] needle complexes that delivers the tir protein into the host cell. Surface arrayed intimin docks the bacterium to the translocated intimin receptor [Tir]. This intimate linkage is the starting point for attachment and effacing lesions. We hypothesize that the chimeric recombinant forms of two of these three effectors, as edible-based immunogens, would reduce colonization of E. coli O157:H7 in the mice model. We constructed a synthetic gene [it] composed of eae [i] and tir [t] attached together by a peptide linker. The synthetic gene [it] was codon optimized based on the tobacco [Nicotiana tobbacum] plant and cloned into plant expression vectors adjacent to CaMV35S promoters for expression in transgenic tobacco plants. The antigen produced in this plant was orally fed to mice. Immunization of the mice model by the transgenic plant that contained the divalent immunogen showed the presence of IgG antibodies against E. coli O157:H7. This method could be an effective tool for protecting against E. coli O157:H7 hemorrhagic colitis