{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,22]],"date-time":"2026-04-22T23:29:03Z","timestamp":1776900543858,"version":"3.51.2"},"reference-count":20,"publisher":"Wiley","license":[{"start":{"date-parts":[[2015,1,1]],"date-time":"2015-01-01T00:00:00Z","timestamp":1420070400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"DOI":"10.13039\/501100003819","name":"Natural Science Foundation of Hubei Province","doi-asserted-by":"publisher","award":["2011-CDB236"],"award-info":[{"award-number":["2011-CDB236"]}],"id":[{"id":"10.13039\/501100003819","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["BioMed Research International"],"published-print":{"date-parts":[[2015]]},"abstract":"<jats:p><jats:italic>Objective.<\/jats:italic>To explore the antiprostate cancer effects of Celastrol on prostate cancer cells\u2019 proliferation, apoptosis, and cell cycle distribution, as well as the correlation to the regulation of hERG.<jats:italic>Methods.<\/jats:italic>DU145 cells were treated with various concentrations of Celastrol (0.25\u201316.0\u2009<jats:italic>\u03bc<\/jats:italic>mol\/L) for 0\u201372 hours. MTT assay was used to evaluate the inhibition effect of Celastrol on the growth of DU145 cells. Cell apoptosis was detected through both Annexin-V FITC\/PI double-labeled cytometry and Hoechst 33258. Cell cycle regulation was examined by a propidium iodide method. Western blot and RT-PCR technologies were applied to assess the expression level of hERG in DU145 cells.<jats:italic>Results.<\/jats:italic>Celastrol presented striking growth inhibition and apoptosis induction potency on DU145 cells<jats:italic>in vitro<\/jats:italic>in a time- and dose-dependent manner. The IC<jats:sub>50<\/jats:sub>value of Celastrol for 24 hours was 2.349 \u00b1 0.213\u2009<jats:italic>\u03bc<\/jats:italic>mol\/L. Moreover, Celastrol induced DU145 cell apoptosis in a cell cycle-dependent manner, which means Celastrol could arrest DU145 cells in G<jats:sub>0<\/jats:sub>\/G<jats:sub>1<\/jats:sub>phase; accordingly, cells in S phase decreased gradually and no obvious changes were found in G<jats:sub>2<\/jats:sub>\/M phase cells. Through transmission electron microscope, apoptotic bodies containing nuclear fragments were found in Celastrol-treated DU145 cells. Overexpression of hERG channel was found in DU145 cells, while Celastrol could downregulate it at both protein and mRNA level in a dose-dependent manner (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\"><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn fontstyle=\"italic\">0.01<\/mml:mn><\/mml:math>).<jats:italic>Conclusions.<\/jats:italic>Celastrol exhibits its antiprostate cancer effects partially through the downregulation of the expression level of hERG channel in DU145 cells, suggesting that Celastrol may be a potential agent against prostate cancer with a mechanism of blocking the hERG channel.<\/jats:p>","DOI":"10.1155\/2015\/308475","type":"journal-article","created":{"date-parts":[[2015,3,19]],"date-time":"2015-03-19T21:20:50Z","timestamp":1426800050000},"page":"1-7","source":"Crossref","is-referenced-by-count":27,"title":["Effect of Celastrol on Growth Inhibition of Prostate Cancer Cells through the Regulation of hERG Channel<i>In 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