<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>11</volume><submitter>Li X</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Celastrol is a major active component of the thunder god vine (&lt;i>Tripterygium wilfordii&lt;/i>) used in traditional Chinese medicine to treat chronic inflammatory and autoimmune diseases. Celastrol inhibits PI3K-Akt-mTOR signaling, which is frequently dysregulated in tumors and critical for tumor-cell proliferation and survival, but the underlying mechanisms are still not fully understood. In the present study, we investigated detailed mechanisms of celastrol inhibition of mTOR signaling in breast cancer cells.&lt;h4>Methods&lt;/h4>First, we evaluated the effect of celastrol on breast cancer-cell growth using MTT assays. Second, we examined the effects of celastrol on mTOR phosphorylation and expression using Western blot. Furthermore, we investigated the cause of mTOR downregul</pubmed_abstract><journal>OncoTargets and therapy</journal><pagination>8977-8985</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6294079</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Celastrol induces ubiquitin-dependent degradation of mTOR in breast cancer cells.</pubmed_title><pmcid>PMC6294079</pmcid><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Wang N</pubmed_authors><pubmed_authors>Kong Q</pubmed_authors><pubmed_authors>Long L</pubmed_authors><pubmed_authors>Cai J</pubmed_authors><pubmed_authors>Zhou D</pubmed_authors><pubmed_authors>Zhou W</pubmed_authors><pubmed_authors>Zhu G</pubmed_authors><pubmed_authors>Yao X</pubmed_authors><pubmed_authors>Hu R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Celastrol induces ubiquitin-dependent degradation of mTOR in breast cancer cells.</name><description>&lt;h4>Background&lt;/h4>Celastrol is a major active component of the thunder god vine (&lt;i>Tripterygium wilfordii&lt;/i>) used in traditional Chinese medicine to treat chronic inflammatory and autoimmune diseases. Celastrol inhibits PI3K-Akt-mTOR signaling, which is frequently dysregulated in tumors and critical for tumor-cell proliferation and survival, but the underlying mechanisms are still not fully understood. In the present study, we investigated detailed mechanisms of celastrol inhibition of mTOR signaling in breast cancer cells.&lt;h4>Methods&lt;/h4>First, we evaluated the effect of celastrol on breast cancer-cell growth using MTT assays. Second, we examined the effects of celastrol on mTOR phosphorylation and expression using Western blot. Furthermore, we investigated the cause of mTOR downregul</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018</publication><modification>2025-04-19T13:57:01.442Z</modification><creation>2019-03-26T22:27:12Z</creation></dates><accession>S-EPMC6294079</accession><cross_references><pubmed>30588010</pubmed><doi>10.2147/OTT.S187315</doi></cross_references></HashMap>