<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sobol A</submitter><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><pagination>1332-41</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4445075</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>230(6)</volume><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</pubmed_abstract><journal>Journal of cellular physiology</journal><pubmed_title>Depletion of Amyloid Precursor Protein (APP) causes G0 arrest in non-small cell lung cancer (NSCLC) cells.</pubmed_title><pmcid>PMC4445075</pmcid><funding_grant_id>R01 CA134503</funding_grant_id><funding_grant_id>CA134503</funding_grant_id><pubmed_authors>Weber MJ</pubmed_authors><pubmed_authors>Galluzzo P</pubmed_authors><pubmed_authors>Bocchetta M</pubmed_authors><pubmed_authors>Sobol A</pubmed_authors><pubmed_authors>Alani S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Depletion of Amyloid Precursor Protein (APP) causes G0 arrest in non-small cell lung cancer (NSCLC) cells.</name><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</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Jun</publication><modification>2025-05-29T19:39:38.044Z</modification><creation>2019-03-27T01:52:13Z</creation></dates><accession>S-EPMC4445075</accession><cross_references><pubmed>25502341</pubmed><doi>10.1002/jcp.24875</doi></cross_references></HashMap>