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Colorectal cancer (CRC) is distinguished by epigenetic elements like DNA methylation, histone modification, histone acetylation and RNA remodeling which is related with genomic instability and tumor initiation. Correspondingly, as a main epigenetic regulation, DNA methylation has an impressive ability in order to be used in CRC targeted therapy. Meaningly, DNA methylation is identified as one of most important epigenetic regulators in gene expression and is considered as a notable potential driver in tumorigenesis and carcinogenesis through gene-silencing of tumor suppressors genes. Abnormal methylation situation, even in the level of promoter regions, does not essentially change the gene expression levels, particularly if the gene was become silenced, leaving the mechanisms of methylation without any response. According to the methylation situation which has a strong eagerness to be highly altered on CpG islands in carcinogenesis and tumorigenesis, considering its epigenetic fluctuations in finding new biomarkers is of great importance. Modifications in DNA methylation pattern and also enrichment of methylated histone signs in the promoter regions of some certain genes like MUTYH, KLF4/6 and WNT1 in different signaling pathways could be a notable key contributors to the upregulation of tumor initiation in CRC. These epigenetic alterations could be employed as a practical diagnostic biomarkers for colorectal cancer. In this review, we will be discuss these fluctuations of MUTYH, KLF4/6 and WNT1 genes in CRC.

Background: The association between depression and inflammatory bowel disease (IBD) has been reported worldwide. Objectives: We aimed to investigate the prevalence of active and inactive IBD depression and its associated risk factors among patients with depression and IBD. Materials & Methods: In this cross-sectional study, demographic data and clinical characteristics of 156 IBD patients referred to Razi Hospital, Rasht City, Iran, were recorded from 2015 to 2016. The Beck depression inventory (BDI) was administered to all patients, and their scores were classified as no, mild, moderate, and severe depression. Modified Truelove and Witts severity index (MTWSI) for ulcerative colitis (UC) and Harvey Bradshaw severity index (HBSI) for Crohn's disease (CD) were used to quantitate IBD activity as active UC (scored =10) and active CD (scored =7). Results: About 35.9% of the patients (n=56) had depression. Patients with active IBD had significantly higher BDI scores than those with inactive IBD (14.41±10.34 vs 10.14±10.28, respectively, P=0.011). Except for income (P=0.001), no significant associations were detected between IBD status and other background variables (P>0.05). No patients in either active or inactive IBD groups had cancers. Based on the severity of depression, the patients were grouped as follows: 64.1% had no depression, 30.1% had mild depression, 5.8% had moderate depression, and 0.0% had severe depression. However, significant positive associations were seen between an increase in depression severity and having autoimmune diseases, a lower education level, and a history of IBD-related surgeries. Conclusion: It seems that patients with active IBD are more depressed than inactive IBD patients. [ABSTRACT FROM AUTHOR]

Purpose: Gastric cancer (GC) is one of the main causes of death from diseases, especially in developing countries. MicroRNAs (miRNAs) are important modulators of the messenger RNAs expression. Among these miRNAs, MiR-143 is a tumor suppressor miRNA and its irregular expression has been revealed in a diversity of malignancies such as GC. Methods: In this study, we have attempted to restore the miR-143 expression in MKN-45 cells by introducing pCMV-miR-143 plasmid vectors. The consequences of exogenous expression of miR-143 on cell proliferation and migration were assessed by MTT and scratch tests, respectively. In addition, the DAPI staining assay was applied for apoptosis quantification. Following miR- 143 transfection, the changes in K-Ras, C-Myc, MMP9, Bax, caspase-3, and caspase-9 mRNA levels were assessed. Results: The results indicated that the enhanced expression of miR-143 had negative effects on MKN-45 cells proliferation and invasion. Moreover, decreased expressions of K-Ras, MMP9, and C-Myc and up-regulation of Bax, caspase-3, and caspase-9 as downstream targets of miR- 143 were recognized. Conclusion: These experimental results indicate that reversing the miR-143 expression, by novel techniques, including miRNA replacement could be considered as an efficient approach to reduce cell survival and metastasis. [ABSTRACT FROM AUTHOR]