<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12(10)</volume><submitter>Jovanovic Stojanov S</submitter><funding>Ministry of Education, Science and Technological Development of the Republic of Serbia</funding><pubmed_abstract>Drug resistance presents a major obstacle to the successful treatment of glioblastoma. Autophagy plays a key role in drug resistance, particularly in relation to targeted therapy, which has prompted the use of autophagy inhibitors to increase the effectiveness of targeted therapeutics. The ability of two Src tyrosine kinase inhibitors, Si306 and its prodrug pro-Si306, to induce autophagy was evaluated in the human glioblastoma cell line U87 and its multidrug-resistant counterpart U87-TxR. Autophagy markers were assessed by flow cytometry, microscopy, and Western blot, and induction of autophagy by these compounds was demonstrated after 3 h as well as 48 h. The effects of Si306 and pro-Si306 on cell proliferation and cell death were examined in the presence or absence of autophagy inhibitio</pubmed_abstract><journal>Life (Basel, Switzerland)</journal><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9605466</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Autophagy Inhibition Enhances Anti-Glioblastoma Effects of Pyrazolo[3,4-d]pyrimidine Tyrosine Kinase Inhibitors</pubmed_title><pmcid>PMC9605466</pmcid><funding_grant_id>451-03-68/2022-14/200007</funding_grant_id><funding_grant_id>451-03-68/2022-14/200042</funding_grant_id><pubmed_authors>Ljujic M</pubmed_authors><pubmed_authors>Schenone S</pubmed_authors><pubmed_authors>Jovanovic Stojanov S</pubmed_authors><pubmed_authors>Pesic M</pubmed_authors><pubmed_authors>Kostic A</pubmed_authors><pubmed_authors>Lupsic E</pubmed_authors><pubmed_authors>Dinic J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Autophagy Inhibition Enhances Anti-Glioblastoma Effects of Pyrazolo[3,4-d]pyrimidine Tyrosine Kinase Inhibitors</name><description>Drug resistance presents a major obstacle to the successful treatment of glioblastoma. Autophagy plays a key role in drug resistance, particularly in relation to targeted therapy, which has prompted the use of autophagy inhibitors to increase the effectiveness of targeted therapeutics. The ability of two Src tyrosine kinase inhibitors, Si306 and its prodrug pro-Si306, to induce autophagy was evaluated in the human glioblastoma cell line U87 and its multidrug-resistant counterpart U87-TxR. Autophagy markers were assessed by flow cytometry, microscopy, and Western blot, and induction of autophagy by these compounds was demonstrated after 3 h as well as 48 h. The effects of Si306 and pro-Si306 on cell proliferation and cell death were examined in the presence or absence of autophagy inhibitio</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Sep</publication><modification>2025-04-26T10:39:55.401Z</modification><creation>2025-04-06T13:28:55.405Z</creation></dates><accession>S-EPMC9605466</accession><cross_references/></HashMap>