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Regulatory network analysis of LINC00472 , a long noncoding RNA downregulated by DNA hypermethylation in colorectal cancer
Author(s) -
Chen L.,
Zhang W.,
Li D.Y.,
Wang X.,
Tao Y.,
Zhang Y.,
Dong C.,
Zhao J.,
Zhang L.,
Zhang X.,
Guo J.,
Zhang X.,
Liao Q.
Publication year - 2018
Publication title -
clinical genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 102
eISSN - 1399-0004
pISSN - 0009-9163
DOI - 10.1111/cge.13245
Subject(s) - dna methylation , epigenetics , biology , colorectal cancer , methylation , cancer research , gene , long non coding rna , cancer , regulation of gene expression , genetics , gene expression , rna
Colorectal cancer (CRC), one of the common malignant cancers in the world, is caused by accumulated alterations of genetic and epigenetic factors over a long period of time. Along with that protein‐coding genes being identified as oncogenes or tumor suppressors in CRC, a number of lncRNAs have also been found to be associated with CRC. Considering the important regulatory role of lncRNAs, the first goal of this study was to identify CRC‐associated lncRNAs from a public database. One such lncRNA, LINC00472 , was verified to be downregulated in CRC cell lines and cancer tissues compared with adjacent tissues. In addition, the down‐regulation of LINC00472 seemed to be caused by DNA hypermethylation at its promoter region. Furthermore, the expression of LINC00472 and DNA methylation of promoter were significantly correlated with clinicopathological features. And DNA hypermethylation of LINC00472 may serve as a better diagnostic biomarker than its expression for CRC. Finally, we predicted the functions of LINC00472 and constructed a regulatory network and found LINC00472 may be involved in cell cycle and cell proliferation processes. Our results may provide a clue to further research into the function and regulatory mechanism of LINC00472 in CRC.