Inverse Modulation of Aurora Kinase A and Topoisomerase IIα in Normal and Tumor Breast Cells upon Knockdown of Mitochondrial ASncmtRNA

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dc.contributor.authorBendek, Maximiliano F.
dc.contributor.authorFitzpatrick, Christopher
dc.contributor.authorJeldes, Emanuel
dc.contributor.authorBoland, Anne
dc.contributor.authorDeleuze, Jean-François
dc.contributor.authorFarfán, Nicole
dc.contributor.authorVillegas, Jaime
dc.contributor.authorNardocci, Gino
dc.contributor.authorMontecino, Martín
dc.contributor.authorBurzio, Luis O.
dc.contributor.authorBurzio, Verónica A.
dc.date.accessioned2023-11-27T19:05:27Z
dc.date.available2023-11-27T19:05:27Z
dc.date.issued2023-10
dc.descriptionIndexación: Scopus.es
dc.description.abstractBreast cancer is currently the most diagnosed form of cancer and the leading cause of death by cancer among females worldwide. We described the family of long non-coding mitochondrial RNAs (ncmtRNAs), comprised of sense (SncmtRNA) and antisense (ASncmtRNA) members. Knockdown of ASncmtRNAs using antisense oligonucleotides (ASOs) induces proliferative arrest and apoptotic death of tumor cells, but not normal cells, from various tissue origins. In order to study the mechanisms underlying this selectivity, in this study we performed RNAseq in MDA-MB-231 breast cancer cells transfected with ASncmtRNA-specific ASO or control-ASO, or left untransfected. Bioinformatic analysis yielded several differentially expressed cell-cycle-related genes, from which we selected Aurora kinase A (AURKA) and topoisomerase IIα (TOP2A) for RT-qPCR and western blot validation in MDA-MB-231 and MCF7 breast cancer cells, as well as normal breast epithelial cells (HMEC). We observed no clear differences regarding mRNA levels but both proteins were downregulated in tumor cells and upregulated in normal cells. Since these proteins play a role in genomic integrity, this inverse effect of ASncmtRNA knockdown could account for tumor cell downfall whilst protecting normal cells, suggesting this approach could be used for genomic protection under cancer treatment regimens or other scenarios.es
dc.description.urihttps://www-scopus-com.recursosbiblioteca.unab.cl/record/display.uri?eid=2-s2.0-85175326324&origin=resultslist&sort=plf-f&src=s&nlo=&nlr=&nls=&sid=3271b1f2e3093c41a16235165adce769&sot=aff&sdt=cl&cluster=scofreetoread%2c%22all%22%2ct&sl=61&s=AF-ID%28%22Universidad+Andr%c3%a9s+Bello%22+60002636%29+AND+SUBJAREA%28BIOC%29&relpos=11&citeCnt=0&searchTerm=
dc.identifier.citationNon-coding RNA Open Access Volume 9, Issue 5 October 2023 Article number 59es
dc.identifier.doi10.3390/ncrna9050059
dc.identifier.issn2311553X
dc.identifier.urihttps://repositorio.unab.cl/xmlui/handle/ria/54167
dc.language.isoenes
dc.publisherMDPIes
dc.rights.licenseCC BY 4.0 DEED Attribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectAntisense therapyes
dc.subjectAurora kinase A.es
dc.subjectBreast canceres
dc.subjectncRNAes
dc.subjectToposiomerase IIαes
dc.titleInverse Modulation of Aurora Kinase A and Topoisomerase IIα in Normal and Tumor Breast Cells upon Knockdown of Mitochondrial ASncmtRNAes
dc.typeArtículoes
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