{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chakraborty A"],"funding":["SiRIC-Curie program - SiRIC","Institut National du Cancer","Agence Nationale de la Recherche","Institut Curie","France Génomique Consortium","ICGex NGS","Fondation pour la Recherche Médicale","Ministère de l'Enseignement Supérieur et de la Recherche","Canceropôle Ile-de-France,","Ligue Nationale Contre le Cancer"],"pagination":["1271-1284"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9341504"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["32(7)"],"pubmed_abstract":["Intronic polyadenylation (IPA) isoforms, which contain alternative last exons, are widely regulated in various biological processes and by many factors. However, little is known about their cytoplasmic regulation and translational status. In this study, we provide the first evidence that the genome-wide patterns of IPA isoform regulation during a biological process can be very distinct between the transcriptome and translatome, and between the nucleus and cytosol. Indeed, by 3'-seq analyses on breast cancer cells, we show that the genotoxic anticancer drug, doxorubicin, preferentially down-regulates the IPA to the last-exon (IPA:LE) isoform ratio in whole cells (as previously reported) but preferentially up-regulates it in polysomes. We further show that in nuclei, doxorubicin almost exclu"],"journal":["Genome research"],"pubmed_title":["Compartment-specific and ELAVL1-coordinated regulation of intronic polyadenylation isoforms by doxorubicin."],"pmcid":["PMC9341504"],"funding_grant_id":["2015-141","DBI20141231314","ANR-10-EQPX-03","INCa-DGOS-4654","ANR-10-INBS-09-08"],"pubmed_authors":["Taricco N","Dutertre M","Gestraud P","Relier S","Chakraborty A","Servant N","Martineau S","Heneman-Masurel A","Inga A","Vagner S","Alaeitabar T","Cadix M","Labbe CM","Devaux A"],"additional_accession":[]},"is_claimable":false,"name":"Compartment-specific and ELAVL1-coordinated regulation of intronic polyadenylation isoforms by doxorubicin.","description":"Intronic polyadenylation (IPA) isoforms, which contain alternative last exons, are widely regulated in various biological processes and by many factors. However, little is known about their cytoplasmic regulation and translational status. In this study, we provide the first evidence that the genome-wide patterns of IPA isoform regulation during a biological process can be very distinct between the transcriptome and translatome, and between the nucleus and cytosol. Indeed, by 3'-seq analyses on breast cancer cells, we show that the genotoxic anticancer drug, doxorubicin, preferentially down-regulates the IPA to the last-exon (IPA:LE) isoform ratio in whole cells (as previously reported) but preferentially up-regulates it in polysomes. We further show that in nuclei, doxorubicin almost exclu","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jul","modification":"2026-05-09T22:38:57.275Z","creation":"2025-02-19T03:26:34.961Z"},"accession":"S-EPMC9341504","cross_references":{"pubmed":["35858751"],"doi":["10.1101/gr.276192.121"]}}