{"entity": "researcher", "timestamp": "2026-08-20T21:37:46.439Z", "family": "Frankel", "given": "Lisa B", "initials": "LB", "orcid": "0000-0001-7249-3607", "affiliations": ["Danish Cancer Society Research Center, Copenhagen, Denmark.", "Biotech Research and Innovation Centre, University of Copenhagen, Copenhagen, Denmark."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/3fe68b077dee407c8a16308fc065026b.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/3fe68b077dee407c8a16308fc065026b"}}, "publications": [{"entity": "publication", "iuid": "fd0b26c5530349c98efc9cc12fab3724", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/fd0b26c5530349c98efc9cc12fab3724.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/fd0b26c5530349c98efc9cc12fab3724"}}, "title": "eIF4A3 regulates the TFEB-mediated transcriptional response via GSK3B to control autophagy.", "authors": [{"family": "Sakellariou", "given": "Despoina", "initials": "D", "orcid": "0000-0001-5894-7879", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/cbabb9948ef74a3a805256973c2ecf8d.json"}}, {"family": "Tiberti", "given": "Matteo", "initials": "M"}, {"family": "Kleiber", "given": "Thomas H", "initials": "TH"}, {"family": "Blazquez", "given": "Lorea", "initials": "L"}, {"family": "L\u00f3pez", "given": "Aida Rodr\u00edguez", "initials": "AR"}, {"family": "Abildgaard", "given": "Marie Holm", "initials": "MH"}, {"family": "Lubas", "given": "Michal", "initials": "M"}, {"family": "Bartek", "given": "Jiri", "initials": "J"}, {"family": "Papaleo", "given": "Elena", "initials": "E"}, {"family": "Frankel", "given": "Lisa B", "initials": "LB", "orcid": "0000-0001-7249-3607", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3fe68b077dee407c8a16308fc065026b.json"}}], "type": "journal article", "published": "2021-12-00", "journal": {"title": "Cell Death Differ.", "issn": "1476-5403", "volume": "28", "issue": "12", "pages": "3344-3356", "issn-l": "1350-9047"}, "abstract": "During autophagy, the coordinated actions of autophagosomes and lysosomes result in the controlled removal of damaged intracellular organelles and superfluous substrates. The evolutionary conservation of this process and its requirement for maintaining cellular homeostasis emphasizes the need to better dissect the pathways governing its molecular regulation. In our previously performed high-content screen, we assessed the effect of 1530 RNA-binding proteins on autophagy. Among the top regulators, we identified the eukaryotic translation initiation factor 4A-3 (eIF4A3). Here we show that depletion of eIF4A3 leads to a potent increase in autophagosome and lysosome biogenesis and an enhanced autophagic flux. This is mediated by the key autophagy transcription factor, TFEB, which becomes dephosphorylated and translocates from the cytoplasm to the nucleus where it elicits an integrated transcriptional response. We further identified an exon-skipping event in the transcript encoding for the direct TFEB kinase, GSK3B, which leads to a reduction in GSK3B expression and activity. Through analysis of TCGA data, we found a significant upregulation of eIF4A3 expression across several cancer types and confirmed the potential relevance of this newly identified signaling axis in human tumors. Hence, our data suggest a previously unrecognized role for eIF4A3 as a gatekeeper of autophagy through the control of TFEB activation, revealing a new mechanism for autophagy regulation.", "doi": "10.1038/s41418-021-00822-y", "pmid": "34158631", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8630043"}, {"db": "pii", "key": "10.1038/s41418-021-00822-y"}], "notes": [], "created": "2026-08-20T08:49:17.779Z", "modified": "2026-08-20T08:49:17.887Z"}, {"entity": "publication", "iuid": "8f2caf91ad654fa19b53bfbbf0da76ca", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/8f2caf91ad654fa19b53bfbbf0da76ca.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/8f2caf91ad654fa19b53bfbbf0da76ca"}}, "title": "Autophagy role(s) in response to oncogenes and DNA replication stress.", "authors": [{"family": "Vanzo", "given": "Riccardo", "initials": "R"}, {"family": "Bartkova", "given": "Jirina", "initials": "J"}, {"family": "Merchut-Maya", "given": "Joanna Maria", "initials": "JM"}, {"family": "Hall", "given": "Arnaldur", "initials": "A"}, {"family": "Bouchal", "given": "Jan", "initials": "J"}, {"family": "Dyrskj\u00f8t", "given": "Lars", "initials": "L"}, {"family": "Frankel", "given": "Lisa B", "initials": "LB", "orcid": "0000-0001-7249-3607", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3fe68b077dee407c8a16308fc065026b.json"}}, {"family": "Gorgoulis", "given": "Vassilis", "initials": "V"}, {"family": "Maya-Mendoza", "given": "Apolinar", "initials": "A", "orcid": "0000-0001-7452-9896", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/8120d9952114478b9909d9906e0dd543.json"}}, {"family": "J\u00e4\u00e4ttel\u00e4", "given": "Marja", "initials": "M", "orcid": "0000-0001-5950-7111", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ad3653231c9d4886b5ffefc302030fd1.json"}}, {"family": "Bartek", "given": "Jiri", "initials": "J"}], "type": "journal article", "published": "2020-03-00", "journal": {"title": "Cell Death Differ.", "issn": "1476-5403", "volume": "27", "issue": "3", "pages": "1134-1153", "issn-l": "1350-9047"}, "abstract": "Autophagy is an evolutionarily conserved process that captures aberrant intracellular proteins and/or damaged organelles for delivery to lysosomes, with implications for cellular and organismal homeostasis, aging and diverse pathologies, including cancer. During cancer development, autophagy may play both tumour-supporting and tumour-suppressing roles. Any relationships of autophagy to the established oncogene-induced replication stress (RS) and the ensuing DNA damage response (DDR)-mediated anti-cancer barrier in early tumorigenesis remain to be elucidated. Here, assessing potential links between autophagy, RS and DDR, we found that autophagy is enhanced in both early and advanced stages of human urinary bladder and prostate tumorigenesis. Furthermore, a high-content, single-cell-level microscopy analysis of human cellular models exposed to diverse genotoxic insults showed that autophagy is enhanced in cells that experienced robust DNA damage, independently of the cell-cycle position. Oncogene- and drug-induced RS triggered first DDR and later autophagy. Unexpectedly, genetic inactivation of autophagy resulted in RS, despite cellular retention of functional mitochondria and normal ROS levels. Moreover, recovery from experimentally induced RS required autophagy to support DNA synthesis. Consistently, RS due to the absence of autophagy could be partly alleviated by exogenous supply of deoxynucleosides. Our results highlight the importance of autophagy for DNA synthesis, suggesting that autophagy may support cancer progression, at least in part, by facilitating tumour cell survival and fitness under replication stress, a feature shared by most malignancies. These findings have implications for better understanding of the role of autophagy in tumorigenesis, as well as for attempts to manipulate autophagy as an anti-tumour therapeutic strategy.", "doi": "10.1038/s41418-019-0403-9", "pmid": "31409894", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC7206042"}, {"db": "pii", "key": "10.1038/s41418-019-0403-9"}], "notes": [], "created": "2026-08-20T08:49:10.122Z", "modified": "2026-08-20T08:49:10.290Z"}]}