The potential regulation of the miR-17-92a cluster by miR-21.
- Publisher:
- PERGAMON-ELSEVIER SCIENCE LTD
- Publication Type:
- Journal Article
- Citation:
- Int J Biochem Cell Biol, 2025, 178, pp. 106705
- Issue Date:
- 2025-01
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Hill, M | |
dc.contributor.author | Stapleton, S | |
dc.contributor.author | Nguyen, PT | |
dc.contributor.author |
Sais, D |
|
dc.contributor.author | Deutsch, F | |
dc.contributor.author | Gay, VC | |
dc.contributor.author | Marsh, DJ | |
dc.contributor.author |
Tran, N |
|
dc.date.accessioned | 2025-01-06T00:25:04Z | |
dc.date.available | 2024-11-26 | |
dc.date.available | 2025-01-06T00:25:04Z | |
dc.date.issued | 2025-01 | |
dc.identifier.citation | Int J Biochem Cell Biol, 2025, 178, pp. 106705 | |
dc.identifier.issn | 1357-2725 | |
dc.identifier.issn | 1878-5875 | |
dc.identifier.uri | http://hdl.handle.net/10453/182980 | |
dc.description.abstract | MicroRNAs (miRNA,miRs) are small noncoding RNAs that are ubiquitously expressed in all mammalian cells. Their primary function is the regulation of nascent RNA transcripts by direct binding to regions on the target. There is now exciting data to suggest that these miRNAs can bind to other miRNAs, and this may have a broader impact on gene regulation in disease states. The oncomiR miR-21 is one of the highest-expressing miRNAs in cancer cells, and in this study, we characterise which miRNAs could be potential targets of miR-21. In cancer cells delivered with a miR-21 mimic, there was an observable shift of the miRNA milieu. We demonstrate that the miR-17-92a cluster, which harbours six miRNA members, may be a target for miR-21 regulation. Additionally, the primary transcript of miR-17-92a was reduced in the presence of miR-21. In the broader context of miR:miR regulation, overexpression of miR-21 shifted the expression of more than 150 miRNAs, including those known to regulate genes in cancer pathways such as the MAPK signalling and FoxO pathways. This study expands upon our limited understanding of miR:miR regulatory network and reinforces the concept that miRNAs can regulate each other, thereby influencing broader gene networks. | |
dc.format | Print-Electronic | |
dc.language | eng | |
dc.publisher | PERGAMON-ELSEVIER SCIENCE LTD | |
dc.relation.ispartof | Int J Biochem Cell Biol | |
dc.relation.isbasedon | 10.1016/j.biocel.2024.106705 | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | 0601 Biochemistry and Cell Biology, 1101 Medical Biochemistry and Metabolomics, 1116 Medical Physiology | |
dc.subject.classification | Biochemistry & Molecular Biology | |
dc.subject.classification | 3101 Biochemistry and cell biology | |
dc.subject.classification | 3205 Medical biochemistry and metabolomics | |
dc.subject.mesh | MicroRNAs | |
dc.subject.mesh | Humans | |
dc.subject.mesh | RNA, Long Noncoding | |
dc.subject.mesh | Gene Expression Regulation, Neoplastic | |
dc.subject.mesh | Multigene Family | |
dc.subject.mesh | Cell Line, Tumor | |
dc.subject.mesh | Cell Line, Tumor | |
dc.subject.mesh | Humans | |
dc.subject.mesh | MicroRNAs | |
dc.subject.mesh | Gene Expression Regulation, Neoplastic | |
dc.subject.mesh | Multigene Family | |
dc.subject.mesh | RNA, Long Noncoding | |
dc.title | The potential regulation of the miR-17-92a cluster by miR-21. | |
dc.type | Journal Article | |
utslib.citation.volume | 178 | |
utslib.location.activity | Netherlands | |
utslib.for | 0601 Biochemistry and Cell Biology | |
utslib.for | 1101 Medical Biochemistry and Metabolomics | |
utslib.for | 1116 Medical Physiology | |
pubs.organisational-group | University of Technology Sydney | |
pubs.organisational-group | University of Technology Sydney/Faculty of Engineering and Information Technology | |
pubs.organisational-group | University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | University of Technology Sydney/Faculty of Science/School of Life Sciences | |
pubs.organisational-group | University of Technology Sydney/Faculty of Engineering and Information Technology/School of Biomedical Engineering | |
pubs.organisational-group | University of Technology Sydney/Faculty of Engineering and Information Technology/School of Electrical and Data Engineering | |
pubs.organisational-group | University of Technology Sydney/UTS Groups | |
pubs.organisational-group | University of Technology Sydney/UTS Groups/Centre for Health Technologies (CHT) | |
pubs.organisational-group | University of Technology Sydney/UTS Groups/The Trustworthy Digital Society | |
utslib.copyright.status | open_access | * |
dc.rights.license | This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/ | |
dc.date.updated | 2025-01-06T00:25:01Z | |
pubs.publication-status | Published | |
pubs.volume | 178 |
Abstract:
MicroRNAs (miRNA,miRs) are small noncoding RNAs that are ubiquitously expressed in all mammalian cells. Their primary function is the regulation of nascent RNA transcripts by direct binding to regions on the target. There is now exciting data to suggest that these miRNAs can bind to other miRNAs, and this may have a broader impact on gene regulation in disease states. The oncomiR miR-21 is one of the highest-expressing miRNAs in cancer cells, and in this study, we characterise which miRNAs could be potential targets of miR-21. In cancer cells delivered with a miR-21 mimic, there was an observable shift of the miRNA milieu. We demonstrate that the miR-17-92a cluster, which harbours six miRNA members, may be a target for miR-21 regulation. Additionally, the primary transcript of miR-17-92a was reduced in the presence of miR-21. In the broader context of miR:miR regulation, overexpression of miR-21 shifted the expression of more than 150 miRNAs, including those known to regulate genes in cancer pathways such as the MAPK signalling and FoxO pathways. This study expands upon our limited understanding of miR:miR regulatory network and reinforces the concept that miRNAs can regulate each other, thereby influencing broader gene networks.
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