A genomic screen for long noncoding RNA genes epigenetically silenced by aberrant DNA methylation in colorectal cancer

Kumegawa, Kohei; Maruyama, Reo; Yamamoto, Eiko; Ashida, Masami; Kitajima, Hiroshi; Tsuyada, Akihiro; Niinuma, Takeshi; Kai, Masahiro; Yamano, Hiro‐o; Sugai, Tamotsu; Tokino, Takashi; Shinomura, Yasuhisa; Imai, Kohzoh; Suzuki, Hiromu

doi:10.1038/srep26699

Cited by 36 publications

(31 citation statements)

References 42 publications

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“…We performed the pathway enrichment analysis to understand the potential biological processes of AML. Our results showed that lncRNAs are regulated by cis-or trans-factors such as DNA methylation or transcription factors, which is similar to coding genes [33,34]. Interestingly, the distributions of TFBSs were different between upregulated and downregulated lncRNAs.…”

Section: Resultsmentioning

confidence: 68%

Genome-wide characterization of lncRNAs in acute myeloid leukemia

Lei

Xia

Liu

et al. 2017

Briefings in Bioinformatics

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Long noncoding RNAs (lncRNAs) are a large family of noncoding RNAs that play a critical role in various normal bioprocesses as well as tumorigenesis. However, the expression patterns and biological functions of lncRNAs in acute leukemia have not been well studied. Here, we performed transcriptome-wide lncRNA expression profiling of acute myeloid leukemia (AML) patient samples, along with non-leukemia control hematopoietic samples. We found that lncRNAs were differentially expressed in AML samples relative to control samples. Notably, we identified that lncRNAs upregulated in AML (relative to the control samples) are associated with a lower degree of DNA methylation and a higher ratio of being bound by transcription factors such as SP1, STAT4, ATF-2 and ELK-1 compared with those downregulated in AML. Moreover, an enrichment of H3K4me3 and a depletion of H3K27me3 were observed in upregulated lncRNAs in AML. Expression patterns of three types of lncRNAs (antisense, enhancer and intergenic lncRNAs) have previously been characterized. Of the identified lncRNAs, we found that high expression level lncRNA LOC285758 is associated with the poor prognosis in AML patients. Furthermore, we found that LOC285758 regulates proliferation of AML cell lines by enhancing the expression of HDAC2, a key factor in carcinogenesis. Collectively, our study depicts a landscape of important lncRNAs in AML and provides novel potential therapeutic targets and prognostic markers for AML treatment.

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Section: Resultsmentioning

confidence: 68%

Genome-wide characterization of lncRNAs in acute myeloid leukemia

Lei

Xia

Liu

et al. 2017

Briefings in Bioinformatics

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“…In recent years, a number of lncRNAs with abnormal DNA methylation level in CRC were found. For example, a genome‐wide analysis of histone modifications in CRC cells found that the transcription start sites of 1027 lncRNA genes acquired trimethylation of histone H3 lysine 4 (H3K4me3) after DNA demethylation, among which 22 lncRNAs were silenced by DNA hypermethylation in CRC . In our previous study, we also identified 761 DNA hypermethylated lncRNAs in CRC, which indicated LINC00472 may be regulated by DNA hypermethylation at its promoter .…”

Section: Introductionmentioning

confidence: 91%

Regulatory network analysis of LINC00472, a long noncoding RNA downregulated by DNA hypermethylation in colorectal cancer

Chen

Zhang

et al. 2018

Clinical Genetics

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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.

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“…LncRNAs are evolutionarily conserved and numerous reports have demonstrated that they exert an important role in cell proliferation, differentiation, and immune response . These responses occur at different molecular levels, such as chromatin modification , DNA methylation , gene imprinting , RNA processing , and epigenetic regulation . LncRNAs have been highlighted as key components of the cancer transcriptome; therefore, it is reasonable to speculate that, depending on the circumstances, they may function as oncogenes, tumor suppressors, or both.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of long noncoding RNA TUG1 promotes cervical cancer cell proliferation and migration

Sun

Mao

et al. 2017

Cancer Medicine

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Long noncoding RNAs (lncRNAs), a novel class of transcripts that have critical roles in carcinogenesis and progression, have emerged as important gene expression modulators. Recent evidence indicates that lncRNA taurine-upregulated gene 1 (TUG1) functions as an oncogene in numerous types of human cancers. However, its function in the development of cervical cancer remains unknown. The aim of this research was to investigate the clinical significance and biological functions of TUG1 in cervical cancer. TUG1 was found to be significantly upregulated in cervical cancer tissues and four cervical cancer cell lines by quantitative real-time polymerase chain reaction (qRT-PCR). Elevated TUG1 expression was correlated with larger tumor size, advanced international federation of gynecology and obstetrics (FIGO) stage, poor differentiation, and lymph node metastasis. Furthermore, knockdown of TUG1 suppressed cell proliferation with activation of apoptosis, in part by regulating the expression of Bcl-2 and caspase-3. Silencing of TUG1 inhibited cell migration and invasion via the progression of epithelial-mesenchymal transition (EMT). Taken together, our findings indicate that TUG1 acts as an oncogene in cervical cancer and may represent a novel therapeutic target. Cancer Medicine Open Access 472

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A genomic screen for long noncoding RNA genes epigenetically silenced by aberrant DNA methylation in colorectal cancer

Cited by 36 publications

References 42 publications

Genome-wide characterization of lncRNAs in acute myeloid leukemia

Genome-wide characterization of lncRNAs in acute myeloid leukemia

Regulatory network analysis of LINC00472, a long noncoding RNA downregulated by DNA hypermethylation in colorectal cancer

Upregulation of long noncoding RNA TUG1 promotes cervical cancer cell proliferation and migration

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