{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Morra F"],"funding":["NIA NIH HHS"],"pagination":["12697-709"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4494967"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["6(14)"],"pubmed_abstract":["CCDC6 gene product is a pro-apoptotic protein substrate of ATM, whose loss or inactivation enhances tumour progression. In primary tumours, the impaired function of CCDC6 protein has been ascribed to CCDC6 rearrangements and to somatic mutations in several neoplasia. Recently, low levels of CCDC6 protein, in NSCLC, have been correlated with tumor prognosis. However, the mechanisms responsible for the variable levels of CCDC6 in primary tumors have not been described yet.We show that CCDC6 turnover is regulated in a cell cycle dependent manner. CCDC6 undergoes a cyclic variation in the phosphorylated status and in protein levels that peak at G2 and decrease in mitosis. The reduced stability of CCDC6 in the M phase is dependent on mitotic kinases and on degron motifs that are present in CCDC"],"journal":["Oncotarget"],"pubmed_title":["FBXW7 and USP7 regulate CCDC6 turnover during the cell cycle and affect cancer drugs susceptibility in NSCLC."],"pmcid":["PMC4494967"],"funding_grant_id":["K01 AG041218"],"pubmed_authors":["Morra F","Monaco G","Cerrato A","Paladino S","Guggino G","Poser I","Luise C","Staibano S","Chiariello M","Denning K","Merolla F","Visconti R","Ilardi G","Claudio PP","Colecchia D","Inuzuka H","Monaco R","Celetti A"],"additional_accession":[]},"is_claimable":false,"name":"FBXW7 and USP7 regulate CCDC6 turnover during the cell cycle and affect cancer drugs susceptibility in NSCLC.","description":"CCDC6 gene product is a pro-apoptotic protein substrate of ATM, whose loss or inactivation enhances tumour progression. In primary tumours, the impaired function of CCDC6 protein has been ascribed to CCDC6 rearrangements and to somatic mutations in several neoplasia. Recently, low levels of CCDC6 protein, in NSCLC, have been correlated with tumor prognosis. However, the mechanisms responsible for the variable levels of CCDC6 in primary tumors have not been described yet.We show that CCDC6 turnover is regulated in a cell cycle dependent manner. CCDC6 undergoes a cyclic variation in the phosphorylated status and in protein levels that peak at G2 and decrease in mitosis. The reduced stability of CCDC6 in the M phase is dependent on mitotic kinases and on degron motifs that are present in CCDC","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 May","modification":"2025-06-01T01:56:04.726Z","creation":"2025-06-01T01:56:04.726Z"},"accession":"S-EPMC4494967","cross_references":{"pubmed":["25885523"],"doi":["10.18632/oncotarget.3708"]}}