<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>65(2)</volume><submitter>Zhang Y</submitter><pubmed_abstract>&lt;h4>Purpose&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/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.&lt;h4>Conclusions&lt;/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.</pubmed_abstract><journal>Investigative ophthalmology &amp; visual science</journal><pagination>34</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10901251</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Antitumoral Potential of the Histone Demethylase Inhibitor GSK-J4 in Retinoblastoma.</pubmed_title><pmcid>PMC10901251</pmcid><pubmed_authors>Yang H</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Huang G</pubmed_authors><pubmed_authors>Xu C</pubmed_authors><pubmed_authors>Wu W</pubmed_authors></additional><is_claimable>false</is_claimable><name>Antitumoral Potential of the Histone Demethylase Inhibitor GSK-J4 in Retinoblastoma.</name><description>&lt;h4>Purpose&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/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.&lt;h4>Conclusions&lt;/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.</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Feb</publication><modification>2025-04-22T06:34:35.408Z</modification><creation>2025-04-05T21:49:33.386Z</creation></dates><accession>S-EPMC10901251</accession><cross_references><pubmed>38393716</pubmed><doi>10.1167/iovs.65.2.34</doi></cross_references></HashMap>