دورية أكاديمية
Evolutionarily conserved enhancer-associated features within the MYEOV locus suggest a regulatory role for this non-coding DNA region in cancer.
| العنوان: | Evolutionarily conserved enhancer-associated features within the MYEOV locus suggest a regulatory role for this non-coding DNA region in cancer. |
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| المؤلفون: | Davidson BSA; Biosciences Institute, Newcastle University, Newcastle upon Tyne, United Kingdom., Arcila-Galvis JE; Biosciences Institute, Newcastle University, Newcastle upon Tyne, United Kingdom., Trevisan-Herraz M; Biosciences Institute, Newcastle University, Newcastle upon Tyne, United Kingdom., Mikulasova A; Biosciences Institute, Newcastle University, Newcastle upon Tyne, United Kingdom., Brackley CA; SUPA, School of Physics and Astronomy, University of Edinburgh, Edinburgh, United Kingdom., Russell LJ; Biosciences Institute, Newcastle University, Newcastle upon Tyne, United Kingdom., Rico D; Biosciences Institute, Newcastle University, Newcastle upon Tyne, United Kingdom.; CABIMER, CSIC-Universidad de Sevilla-Universidad Pablo de Olavide-Junta de Andalucía, Seville, Spain. |
| المصدر: | Frontiers in cell and developmental biology [Front Cell Dev Biol] 2024 Jul 30; Vol. 12, pp. 1294510. Date of Electronic Publication: 2024 Jul 30 (Print Publication: 2024). |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Frontiers Media S.A Country of Publication: Switzerland NLM ID: 101630250 Publication Model: eCollection Cited Medium: Print ISSN: 2296-634X (Print) Linking ISSN: 2296634X NLM ISO Abbreviation: Front Cell Dev Biol Subsets: PubMed not MEDLINE |
| أسماء مطبوعة: | Original Publication: Lausanne : Frontiers Media S.A., [2013]- |
| مستخلص: | The myeloma overexpressed gene ( MYEOV ) has been proposed to be a proto-oncogene due to high RNA transcript levels found in multiple cancers, including myeloma, breast, lung, pancreas and esophageal cancer. The presence of an open reading frame (ORF) in humans and other primates suggests protein-coding potential. Yet, we still lack evidence of a functional MYEOV protein. It remains undetermined how MYEOV overexpression affects cancerous tissues. In this work, we show that MYEOV has likely originated and may still function as an enhancer, regulating CCND1 and LTO1 . Firstly, MYEOV 3' enhancer activity was confirmed in humans using publicly available ATAC-STARR-seq data, performed on B-cell-derived GM12878 cells. We detected enhancer histone marks H3K4me1 and H3K27ac overlapping MYEOV in multiple healthy human tissues, which include B cells, liver and lung tissue. The analysis of 3D genome datasets revealed chromatin interactions between a MYEOV-3 ' -putative enhancer and the proto-oncogene CCND1 . BLAST searches and multi-sequence alignment results showed that DNA sequence from this human enhancer element is conserved from the amphibians/amniotes divergence, with a 273 bp conserved region also found in all mammals, and even in chickens, where it is consistently located near the corresponding CCND1 orthologues. Furthermore, we observed conservation of an active enhancer state in the MYEOV orthologues of four non-human primates, dogs, rats, and mice. When studying this homologous region in mice, where the ORF of MYEOV is absent, we not only observed an enhancer chromatin state but also found interactions between the mouse enhancer homolog and Ccnd1 using 3D-genome interaction data. This is similar to the interaction observed in humans and, interestingly, coincides with CTCF binding sites in both species. Taken together, this suggests that MYEOV is a primate-specific gene with a de novo ORF that originated at an evolutionarily older enhancer region. This deeply conserved putative enhancer element could regulate CCND1 in both humans and mice, opening the possibility of studying MYEOV regulatory functions in cancer using non-primate animal models. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2024 Davidson, Arcila-Galvis, Trevisan-Herraz, Mikulasova, Brackley, Russell and Rico.) |
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| فهرسة مساهمة: | Keywords: CCND1 (Cyclin D1); MYEOV; enhancer; evolution; oncogene |
| تواريخ الأحداث: | Date Created: 20240814 Latest Revision: 20240815 |
| رمز التحديث: | 20240815 |
| مُعرف محوري في PubMed: | PMC11319300 |
| DOI: | 10.3389/fcell.2024.1294510 |
| PMID: | 39139450 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 2296-634X |
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| DOI: | 10.3389/fcell.2024.1294510 |