New Studies of the Aberrant Alterations in Fibrillin-1 Methylation During Colorectal Cancer Development

BackgroundFibrillin-1 (FBN1) methylation risk from control to colorectal cancer (CRC), the variation regularities of FBN1 methylation, and DNA methyltransferase (DNMT) catalyzed with FBN1 methylation had not been reported yet; these were all studied in this paper. MethodsFBN1 methylation roles were investigated with big data and meta-analysis. ResultsThe 6 independent studies were searched including 702 tissue and 448 feces. FBN1 methylation frequencies of CRC, adenoma or polyp, and control in tissue were 79.1%, 69.4%, and 2.7%, respectively; those in feces were 74.6%, 50.7%, and 10.8%, respectively. FBN1 methylation of control samples was used as a standard reference; this study showed that ORs (95% CI) of FBN1 methylation in CRC and control tissues were 124.79 (62.86-248.35); those in feces were detected to be 30.87 (16.48-57.85). FBN1 methylation risk in tissue was higher than that in feces; there was a quadratic equation between the methylation rate of tissue and that of feces. There was another quadratic curve in the variation process of FBN1 methylation; this curve reflected the overall metabolism regularity of DNMT. ConclusionsThe transcriptional inactivation of FBN1 gene might start from normal colonic epithelium; the quadratic curve of FBN1 methylation catalyzed by DNMT can gradually produce powerful strength, accelerate expansion, and eventually lead to CRC. The overall metabolism regularity of DNMT maintains the changing process of FBN1 methylation; it has the changing feature of the same quadratic curve. FBN1 methylation is a promising biomarker. FBN1 methylation risk size in feces reflects that in tissue in non-invasive detection.