{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Casalino L"],"funding":["Worldwide Cancer Research"],"pagination":["1878-90"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC1847654"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(7)"],"pubmed_abstract":["Fra-1 is frequently overexpressed in epithelial cancers and implicated in invasiveness. We previously showed that Fra-1 plays crucial roles in RAS transformation in rat thyroid cells and mouse fibroblasts. Here, we report a novel role for Fra-1 as a regulator of mitotic progression in RAS-transformed thyroid cells. Fra-1 expression and phosphorylation are regulated during the cell cycle, peaking at G2/M. Knockdown of Fra-1 caused a proliferative block and apoptosis. Although most Fra-1-knockdown cells accumulated in G2, a fraction of cells entering M-phase underwent abortive cell division and exhibited hallmarks of genomic instability (micronuclei, lagging chromosomes and anaphase bridges). Furthermore, we established a link between Fra-1 and the cell-cycle machinery by identifying cyclin "],"journal":["The EMBO journal"],"pubmed_title":["Fra-1 promotes growth and survival in RAS-transformed thyroid cells by controlling cyclin A transcription."],"pmcid":["PMC1847654"],"funding_grant_id":["02-0347"],"pubmed_authors":["Yaniv M","Weitzman JB","Verde P","Casalino L","Bakiri L","Talotta F","Fusco A"],"additional_accession":[]},"is_claimable":false,"name":"Fra-1 promotes growth and survival in RAS-transformed thyroid cells by controlling cyclin A transcription.","description":"Fra-1 is frequently overexpressed in epithelial cancers and implicated in invasiveness. We previously showed that Fra-1 plays crucial roles in RAS transformation in rat thyroid cells and mouse fibroblasts. Here, we report a novel role for Fra-1 as a regulator of mitotic progression in RAS-transformed thyroid cells. Fra-1 expression and phosphorylation are regulated during the cell cycle, peaking at G2/M. Knockdown of Fra-1 caused a proliferative block and apoptosis. Although most Fra-1-knockdown cells accumulated in G2, a fraction of cells entering M-phase underwent abortive cell division and exhibited hallmarks of genomic instability (micronuclei, lagging chromosomes and anaphase bridges). Furthermore, we established a link between Fra-1 and the cell-cycle machinery by identifying cyclin ","dates":{"release":"2007-01-01T00:00:00Z","publication":"2007 Apr","modification":"2026-03-16T16:42:59.07Z","creation":"2019-03-27T02:03:42Z"},"accession":"S-EPMC1847654","cross_references":{"pubmed":["17347653"],"doi":["10.1038/sj.emboj.7601617"]}}