{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liu Z"],"funding":["Science and Technology Committee of Shanghai","the National Natural Science Foundation of China"],"pagination":["2385517"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11296530"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["25(1)"],"pubmed_abstract":["CDK4 is highly expressed and associated with poor prognosis and decreased survival in advanced neuroblastoma (NB). Targeting CDK4 degradation presents a potentially promising therapeutic strategy compared to conventional CDK4 inhibitors. However, the autophagic degradation of the CDK4 protein and its anti-proliferation effect in NB cells has not been mentioned. We identified autophagy as a new pathway for the degradation of CDK4. Firstly, autophagic degradation of CDK4 is critical for NVP-BEZ235-induced G0/G1 arrest, as demonstrated by the overexpression of CDK4, autophagy inhibition, and blockade of autophagy-related genes. Secondly, we present the first evidence that p62 binds to CDK4 and then enters the autophagy-lysosome to degrade CDK4 in a CTSB-dependent manner in NVP-BEZ235 treated "],"journal":["Cancer biology & therapy"],"pubmed_title":["Autophagic degradation of CDK4 is responsible for G0/G1 cell cycle arrest in NVP-BEZ235-treated neuroblastoma."],"pmcid":["PMC11296530"],"funding_grant_id":["14401901500","82002922"],"pubmed_authors":["Liu Z","Guo Y","Liu SL","Zhang C","Gao FH","Wang HW","Liu F","Wang XY"],"additional_accession":[]},"is_claimable":false,"name":"Autophagic degradation of CDK4 is responsible for G0/G1 cell cycle arrest in NVP-BEZ235-treated neuroblastoma.","description":"CDK4 is highly expressed and associated with poor prognosis and decreased survival in advanced neuroblastoma (NB). Targeting CDK4 degradation presents a potentially promising therapeutic strategy compared to conventional CDK4 inhibitors. However, the autophagic degradation of the CDK4 protein and its anti-proliferation effect in NB cells has not been mentioned. We identified autophagy as a new pathway for the degradation of CDK4. Firstly, autophagic degradation of CDK4 is critical for NVP-BEZ235-induced G0/G1 arrest, as demonstrated by the overexpression of CDK4, autophagy inhibition, and blockade of autophagy-related genes. Secondly, we present the first evidence that p62 binds to CDK4 and then enters the autophagy-lysosome to degrade CDK4 in a CTSB-dependent manner in NVP-BEZ235 treated ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Dec","modification":"2025-04-19T20:46:41.373Z","creation":"2025-02-19T02:27:18.889Z"},"accession":"S-EPMC11296530","cross_references":{"pubmed":["39087955"],"doi":["10.1080/15384047.2024.2385517"]}}