Lnc-ing RNA Expression with Disease Pathogenesis: MALAT1 and ANRIL in Ulcerative Colitis
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EDITORIAL
Lnc‑ing RNA Expression with Disease Pathogenesis: MALAT1 and ANRIL in Ulcerative Colitis Maria Serena Longhi1 · Efi Kokkotou2
© Springer Science+Business Media, LLC, part of Springer Nature 2020
A wealth of studies has provided increasingly robust evidence of the involvement of long noncoding RNAs (lncRNAs) in the pathogenesis of several disease processes. lncRNAs are conventionally defined as transcripts longer than 200 nucleotides that lack protein coding potential. According to the latest version of the NONCODE database, although they can originate from > 96,000 genes in the form of > 172,000 transcripts, only a small percentage of lncRNAs has been annotated. They are localized primarily in the nucleus although they can also be present in the cell cytoplasm and in the extracellular fluids. lncRNAs exert their functions through interactions with chromatin, transcription factors, RNA, and proteins. In inflammatory bowel disease (IBD), although several studies reported differential expression of lncRNAs in ulcerative colitis (UC) or in Crohn’s disease (CD), including DQ786343, ANRIL(CDKN2BAS1), IFNG-AS1, H19, BC012900, MALAT1, LINC01272, HNF4A-AS1, RP11-44K6.2, CCAT1, GAS5, DIO3OS, and KIF9-AS1 [1, 2], the degree of overlap among the dysregulated lncRNAs that have been identified thus far is limited, potentially owing to varying methodological approaches to lncRNA analysis, characteristics of the individual patient cohorts, and most importantly, the small number of samples analyzed. In this issue of Digestive Diseases and Sciences, Zhu and colleagues [3] using a targeted approach examined expression of the lncRNA MALAT (metastasis-associated lung adenocarcinoma transcript1; synonyms HCN, LINC00047, MALAT-1, NCRNA00047, noncoding nuclear-enriched abundant transcript [NEAT]2, PRO1073, and mascRNA) * Efi Kokkotou [email protected] 1
Department of Anesthesia, Critical Care and Pain Medicine, Harvard Medical School, Boston, MA, USA
Department of Medicine, Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
2
and lncRNA ANRIL (antisense noncoding RNA in the INK4 locus; synonyms CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, RP11-145E5.4, and p15AS) in UC using well-characterized samples from a cohort of 76 newly diagnosed and treatment-naïve UC patients and 76 gender- and age-matched healthy volunteers of the same ethnicity. The selection of MALAT1 and ANRIL was based on their previous RNA sequencing data, in which MALAT1 and ANRIL were inversely correlated. The authors reported significant upregulation of MALAT1 and ANRIL in the colonic mucosa of UC patients compared with controls, which for MALAT1 was also reflected in plasma levels. Furthermore, colonic expression of MALAT1 and ANRIL was strongly correlated among the UC patients, a relation that was not apparent among healthy controls. Though the study by Zhu et al. analyzed a relatively large and well-controlled cohort of UC patients who were newly diagnosed and treatmentnaïve, and stud
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