{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["65(2)"],"submitter":["Zhang Y"],"pubmed_abstract":["<h4>Purpose</h4>The purpose of this study was to investigate the antitumor effects of GSK-J4 on retinoblastoma, as well as its related biological functions and molecular mechanisms.<h4>Methods</h4>The antitumor effect of GSK-J4 on retinoblastoma was evaluated by in vitro and in vivo assays. CCK-8, EdU incorporation, and soft agar colony formation assays were performed to examine the effect of GSK-J4 on cell proliferation. Flow cytometry was used to evaluate the effect of GSK-J4 on the cell cycle and apoptosis. RNA-seq and Western blotting were conducted to explore the molecular mechanisms of GSK-J4. An orthotopic xenograft model was established to determine the effect of GSK-J4 on tumor growth.<h4>Results</h4>GSK-J4 significantly inhibited retinoblastoma cell proliferation both in vitro and in vivo, arrested the cell cycle at G2/M phase, and induced apoptosis. Mechanistically, GSK-J4 may suppress retinoblastoma cell growth by regulating the PI3K/AKT/NF-κB signaling pathway.<h4>Conclusions</h4>The antitumor effects of GSK-J4 were noticeable in retinoblastoma and were at least partially mediated by PI3K/AKT/NF-κB pathway suppression. Our study provides a novel strategy for the treatment of retinoblastoma."],"journal":["Investigative ophthalmology & visual science"],"pagination":["34"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10901251"],"repository":["biostudies-literature"],"pubmed_title":["Antitumoral Potential of the Histone Demethylase Inhibitor GSK-J4 in Retinoblastoma."],"pmcid":["PMC10901251"],"pubmed_authors":["Yang H","Zhang Y","Huang G","Xu C","Wu W"],"additional_accession":[]},"is_claimable":false,"name":"Antitumoral Potential of the Histone Demethylase Inhibitor GSK-J4 in Retinoblastoma.","description":"<h4>Purpose</h4>The purpose of this study was to investigate the antitumor effects of GSK-J4 on retinoblastoma, as well as its related biological functions and molecular mechanisms.<h4>Methods</h4>The antitumor effect of GSK-J4 on retinoblastoma was evaluated by in vitro and in vivo assays. CCK-8, EdU incorporation, and soft agar colony formation assays were performed to examine the effect of GSK-J4 on cell proliferation. Flow cytometry was used to evaluate the effect of GSK-J4 on the cell cycle and apoptosis. RNA-seq and Western blotting were conducted to explore the molecular mechanisms of GSK-J4. An orthotopic xenograft model was established to determine the effect of GSK-J4 on tumor growth.<h4>Results</h4>GSK-J4 significantly inhibited retinoblastoma cell proliferation both in vitro and in vivo, arrested the cell cycle at G2/M phase, and induced apoptosis. Mechanistically, GSK-J4 may suppress retinoblastoma cell growth by regulating the PI3K/AKT/NF-κB signaling pathway.<h4>Conclusions</h4>The antitumor effects of GSK-J4 were noticeable in retinoblastoma and were at least partially mediated by PI3K/AKT/NF-κB pathway suppression. Our study provides a novel strategy for the treatment of retinoblastoma.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Feb","modification":"2025-04-22T06:34:35.408Z","creation":"2025-04-05T21:49:33.386Z"},"accession":"S-EPMC10901251","cross_references":{"pubmed":["38393716"],"doi":["10.1167/iovs.65.2.34"]}}