{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["27(4)"],"submitter":["Debsharma S"],"funding":["Science and Engineering Research Board"],"pubmed_abstract":["Gastric cancer (GC) is a deadly malignancy that demands effective therapeutic intervention capitalizing unique drug target/s. Here, we report that indomethacin, a cyclooxygenase non-selective non-steroidal anti-inflammatory drug, arrests GC cell growth by targeting mitochondrial deacetylase Sirtuin 3 (SIRT3). Interaction study revealed that indomethacin competitively inhibited SIRT3 by binding to nicotinamide adenine dinucleotide (NAD)-binding site. The Cancer Genome Atlas data meta-analysis indicated poor prognosis associated with high SIRT3 expression in GC. Further, transcriptome sequencing data of human gastric adenocarcinoma cells revealed that indomethacin treatment severely downregulated SIRT3. Indomethacin-induced SIRT3 downregulation augmented SOD2 and OGG1 acetylation, leading to"],"journal":["iScience"],"pagination":["109384"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10972828"],"repository":["biostudies-literature"],"pubmed_title":["NSAID targets SIRT3 to trigger mitochondrial dysfunction and gastric cancer cell death."],"pmcid":["PMC10972828"],"pubmed_authors":["Saha D","Pal U","Das T","Bindu S","Banerjee C","De R","Debsharma S","Mazumder S","Ghosh Z","Pramanik S","Chandra Maiti N","Bandyopadhyay U","Nag S"],"additional_accession":[]},"is_claimable":false,"name":"NSAID targets SIRT3 to trigger mitochondrial dysfunction and gastric cancer cell death.","description":"Gastric cancer (GC) is a deadly malignancy that demands effective therapeutic intervention capitalizing unique drug target/s. Here, we report that indomethacin, a cyclooxygenase non-selective non-steroidal anti-inflammatory drug, arrests GC cell growth by targeting mitochondrial deacetylase Sirtuin 3 (SIRT3). Interaction study revealed that indomethacin competitively inhibited SIRT3 by binding to nicotinamide adenine dinucleotide (NAD)-binding site. The Cancer Genome Atlas data meta-analysis indicated poor prognosis associated with high SIRT3 expression in GC. Further, transcriptome sequencing data of human gastric adenocarcinoma cells revealed that indomethacin treatment severely downregulated SIRT3. Indomethacin-induced SIRT3 downregulation augmented SOD2 and OGG1 acetylation, leading to","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2026-07-16T04:12:58.502Z","creation":"2025-04-05T23:18:04.874Z"},"accession":"S-EPMC10972828","cross_references":{"pubmed":["38550981"],"doi":["10.1016/j.isci.2024.109384"]}}