{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jang JY"],"funding":["National Research Foundation of Korea"],"pagination":["E96"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6337620"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(1)"],"pubmed_abstract":["We investigated the antitumor activity and action mechanism of MHY440 in AGS human gastric cancer cells. MHY440 inhibited topoisomerase (Topo) Ι activity and was associated with a DNA damage response signaling pathway. It exhibited a stronger anti-proliferative effect on AGS cells relative to Hs27 human foreskin fibroblast cells, and this effect was both time- and concentration-dependent. MHY440 also increased cell arrest in the G2/M phase by decreasing cyclin B1, Cdc2, and Cdc25c, and upregulating p53 and p73. MHY440 induced AGS cell apoptosis through the upregulation of Fas-L, Fas, and Bax as well as the proteolysis of BH3 interacting-domain death agonist and poly(ADP-ribose) polymerase. It also contributed to the loss of mitochondrial membrane potential. The apoptotic cell death induced"],"journal":["Molecules (Basel, Switzerland)"],"pubmed_title":["MHY440, a Novel Topoisomerase Ι Inhibitor, Induces Cell Cycle Arrest and Apoptosis via a ROS-Dependent DNA Damage Signaling Pathway in AGS Human Gastric Cancer Cells."],"pmcid":["PMC6337620"],"funding_grant_id":["2009-0083538","2018R1D1A1B07044648"],"pubmed_authors":["Moon HR","Kim ND","Chung HY","Kang YJ","Kang D","Sung B","Kim MJ","Park C","Jang JY"],"additional_accession":[]},"is_claimable":false,"name":"MHY440, a Novel Topoisomerase Ι Inhibitor, Induces Cell Cycle Arrest and Apoptosis via a ROS-Dependent DNA Damage Signaling Pathway in AGS Human Gastric Cancer Cells.","description":"We investigated the antitumor activity and action mechanism of MHY440 in AGS human gastric cancer cells. MHY440 inhibited topoisomerase (Topo) Ι activity and was associated with a DNA damage response signaling pathway. It exhibited a stronger anti-proliferative effect on AGS cells relative to Hs27 human foreskin fibroblast cells, and this effect was both time- and concentration-dependent. MHY440 also increased cell arrest in the G2/M phase by decreasing cyclin B1, Cdc2, and Cdc25c, and upregulating p53 and p73. MHY440 induced AGS cell apoptosis through the upregulation of Fas-L, Fas, and Bax as well as the proteolysis of BH3 interacting-domain death agonist and poly(ADP-ribose) polymerase. It also contributed to the loss of mitochondrial membrane potential. The apoptotic cell death induced","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Dec","modification":"2026-05-05T06:37:34.483Z","creation":"2019-03-26T22:40:59Z"},"accession":"S-EPMC6337620","cross_references":{"pubmed":["30597845"],"doi":["10.3390/molecules24010096"]}}