{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sobol A"],"funding":["NCI NIH HHS","National Institutes of Health"],"pagination":["1332-41"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4445075"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["230(6)"],"pubmed_abstract":["We recently reported that Amyloid Precursor Protein (APP) regulates global protein synthesis in a variety of human dividing cells, including non-small cell lung cancer (NSCLC) cells. More specifically, APP depletion causes an increase of both cap- and IRES-dependent translation. Since growth and proliferation are tightly coupled processes, here, we asked what effects artificial downregulation of APP could have elicited in NSCLC cells proliferation. APP depletion caused a G0/G1 arrest through destabilization of the cyclin-C protein and reduced pRb phosphorylation at residues Ser802/811. siRNA to cyclin-C mirrored the cell cycle distribution observed when silencing APP. Cells arrested in G0/G1 (and with augmented global protein synthesis) increased their size and underwent a necrotic cell de"],"journal":["Journal of cellular physiology"],"pubmed_title":["Depletion of Amyloid Precursor Protein (APP) causes G0 arrest in non-small cell lung cancer (NSCLC) cells."],"pmcid":["PMC4445075"],"funding_grant_id":["R01 CA134503","CA134503"],"pubmed_authors":["Weber MJ","Galluzzo P","Bocchetta M","Sobol A","Alani S"],"additional_accession":[]},"is_claimable":false,"name":"Depletion of Amyloid Precursor Protein (APP) causes G0 arrest in non-small cell lung cancer (NSCLC) cells.","description":"We recently reported that Amyloid Precursor Protein (APP) regulates global protein synthesis in a variety of human dividing cells, including non-small cell lung cancer (NSCLC) cells. More specifically, APP depletion causes an increase of both cap- and IRES-dependent translation. Since growth and proliferation are tightly coupled processes, here, we asked what effects artificial downregulation of APP could have elicited in NSCLC cells proliferation. APP depletion caused a G0/G1 arrest through destabilization of the cyclin-C protein and reduced pRb phosphorylation at residues Ser802/811. siRNA to cyclin-C mirrored the cell cycle distribution observed when silencing APP. Cells arrested in G0/G1 (and with augmented global protein synthesis) increased their size and underwent a necrotic cell de","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Jun","modification":"2025-05-29T19:39:38.044Z","creation":"2019-03-27T01:52:13Z"},"accession":"S-EPMC4445075","cross_references":{"pubmed":["25502341"],"doi":["10.1002/jcp.24875"]}}