![]() In addition, cheRNAs function at multiple chromatin levels, including chromatin modification ( Khalil et al., 2009), chromosome inactivation ( Brown et al., 1992), nuclear structure changes ( Bergmann and Spector, 2014 Quinodoz and Guttman, 2014 Engreitz et al., 2016), and transcription ( Ponting et al., 2009 Vance and Ponting, 2014). ![]() CheRNAs are lineage specific, which can stimulate gene transcription in cis by promoting contacts to a downstream enhancer ( Werner et al., 2017). ![]() CheRNA can be regarded as a new kind of enhancer RNA, but their strand length, histone modification markers, and strand-specificity are different ( Gayen and Kalantry, 2017). As a unique subgroup of lncRNAs, chromatin-enriched RNAs (cheRNAs) that are generally transcribed by RNA polymerase II and enriched around chromatin, and can transcriptionally activate neighboring genes ( Werner and Ruthenburg, 2015). They are usually located in the nucleus and enriched in chromatin and specific subnuclear compartments ( Sun et al., 2018). LncRNAs constitute a class of functional RNA molecules with a length of more than 200 nucleotides and lacking protein coding ability. Genome-wide association analysis (GWAS) indicates that noncoding genome mutations are relevant to a variety of diseases, including tumors ( Maurano et al., 2012).Īccording to transcriptome analysis, human cells generate a large number of transcripts, of which over 68% were classified as long noncoding RNAs (lncRNAs Iyer et al., 2015). Compared to protein-coding genes, those noncoding genes account for more than 98% of the entire human genome, in which mutations may lead to tumorigenesis. ![]() Studies have shown that somatic copy-number changes ( Beroukhim et al., 2010), epigenetic changes ( Kundaje et al., 2015), and mutations in noncoding regions ( Melton et al., 2015) are deeply associated with tumorigenesis. The reasons of tumor formation are complex and involve many factors, which also increases the difficulty of tumor therapy. It is estimated that approximately 9.6 million people died of cancer in 2018 ( Bray et al., 2018). This review focuses on the mechanisms of cheRNAs in epigenetic regulation and chromatin conformation and discusses the way cheRNAs function in CSCs to deepen the understanding of tumorigenesis and provide novel insight to advance tumor-targeting therapy.Īs one of the main causes of death worldwide, cancer impedes the increase in people’s life expectancy. The critical effect of cancer stem cells (CSCs) on the formation and development of tumors is well known, but the function of cheRNAs in tumorigenesis, especially in CSC proliferation and stemness maintenance, is not yet fully understood. The abnormal transcription of cheRNAs plays an important role in the occurrence of many diseases, particularly tumors. Recent studies have shown that cheRNAs affect chromatin structure and gene expression by recruiting chromatin modifiers or acting as bridges between distal enhancers and promoters. 2Frontier Science Research Center for Stem Cells, Tongji University, Shanghai, ChinaĬhromatin-enriched RNAs (cheRNAs) constitute a special class of long noncoding RNAs (lncRNAs) that are enriched around chromatin and function to activate neighboring or distal gene transcription.1Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Science and Technology, Tongji University, Shanghai, China.Jixing Zhang 1,2, Tianyi Ding 1,2 and He Zhang 1,2 * †
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