{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zolekar A"],"funding":["NIA NIH HHS"],"pagination":["1538-1551"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6288164"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["119(12)"],"pubmed_abstract":["<h4>Background</h4>Although NGLY1 is known as a pivotal enzyme that catalyses the deglycosylation of denatured glycoproteins, information regarding the responses of human cancer and normal cells to NGLY1 suppression is limited.<h4>Methods</h4>We examined how NGLY1 expression affects viability, tumour growth, and responses to therapeutic agents in melanoma cells and an animal model. Molecular mechanisms contributing to NGLY1 suppression-induced anticancer responses were revealed by systems biology and chemical biology studies. Using computational and medicinal chemistry-assisted approaches, we established novel NGLY1-inhibitory small molecules.<h4>Results</h4>Compared with normal cells, NGLY1 was upregulated in melanoma cell lines and patient tumours. NGLY1 knockdown caused melanoma cell de"],"journal":["British journal of cancer"],"pubmed_title":["Stress and interferon signalling-mediated apoptosis contributes to pleiotropic anticancer responses induced by targeting NGLY1."],"pmcid":["PMC6288164"],"funding_grant_id":["T32 AG020494"],"pubmed_authors":["Ho YY","Sampat R","Zolekar A","Liu J","Lin VJT","Emmitte KA","Hayatshahi HS","Liao X","Wang YC","Mishra NM","Hoffmann P","Parab A"],"additional_accession":[]},"is_claimable":false,"name":"Stress and interferon signalling-mediated apoptosis contributes to pleiotropic anticancer responses induced by targeting NGLY1.","description":"<h4>Background</h4>Although NGLY1 is known as a pivotal enzyme that catalyses the deglycosylation of denatured glycoproteins, information regarding the responses of human cancer and normal cells to NGLY1 suppression is limited.<h4>Methods</h4>We examined how NGLY1 expression affects viability, tumour growth, and responses to therapeutic agents in melanoma cells and an animal model. Molecular mechanisms contributing to NGLY1 suppression-induced anticancer responses were revealed by systems biology and chemical biology studies. Using computational and medicinal chemistry-assisted approaches, we established novel NGLY1-inhibitory small molecules.<h4>Results</h4>Compared with normal cells, NGLY1 was upregulated in melanoma cell lines and patient tumours. NGLY1 knockdown caused melanoma cell de","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Dec","modification":"2026-05-05T22:16:28.204Z","creation":"2019-07-25T07:11:38Z"},"accession":"S-EPMC6288164","cross_references":{"pubmed":["30385822"],"doi":["10.1038/s41416-018-0265-9"]}}