ADAR1 Transcriptome editing promotes breast cancer progression through the regulation of cell cycle and DNA damage response
Author
dc.contributor.author
Sagredo, Eduardo A.
Author
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Sagredo, Alfredo I.
Author
dc.contributor.author
Blanco, Alejandro
Author
dc.contributor.author
Rojas De Santiago, Pamela
Author
dc.contributor.author
Rivas, Solange
Author
dc.contributor.author
Assar Cuevas, Rodrigo
Author
dc.contributor.author
Pérez, Paola
Author
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Marcelain Cubillos, Katherine
Author
dc.contributor.author
Armisen Yáñez, Ricardo
Admission date
dc.date.accessioned
2020-06-22T22:52:29Z
Available date
dc.date.available
2020-06-22T22:52:29Z
Publication date
dc.date.issued
2020
Cita de ítem
dc.identifier.citation
BBA - Molecular Cell Research 1867 (2020) 118716
es_ES
Identifier
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10.1016/j.bbamcr.2020.118716
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/175630
Abstract
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RNA editing has emerged as a novel mechanism in cancer progression. The double stranded RNA-specific adenosine deaminase (ADAR) modifies the expression of an important proportion of genes involved in cell cycle control, DNA damage response (DDR) and transcriptional processing, suggesting an important role of ADAR in transcriptome regulation. Despite the phenotypic implications of ADAR deregulation in several cancer models, the role of ADAR on DDR and proliferation in breast cancer has not been fully addressed. Here, we show that ADAR expression correlates significantly with clinical outcomes and DDR, cell cycle and proliferation mRNAs of previously reported edited transcripts in breast cancer patients. ADAR's knock-down in a breast cancer cell line produces stability changes of mRNAs involved in DDR and DNA replication. Breast cancer cells with reduced levels of ADAR show a decreased viability and an increase in apoptosis, displaying a significant decrease of their DDR activation, compared to control cells. These results suggest that ADAR plays an important role in breast cancer progression through the regulation of mRNA stability and expression of those genes involved in proliferation and DDR impacting the viability of breast cancer cells.
es_ES
Patrocinador
dc.description.sponsorship
Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT)
CONICYT FONDECYT
3190738
1151446
1151435
Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT)
21130361
21161206