Article(id=1222469711988777366, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1222469705873481976, articleNumber=null, orderNo=null, doi=10.16438/j.0513-4870.2019-0672, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1566403200000, receivedDateStr=2019-08-22, revisedDate=1569340800000, revisedDateStr=2019-09-25, acceptedDate=null, acceptedDateStr=null, onlineDate=1769389091727, onlineDateStr=2026-01-26, pubDate=1570809600000, pubDateStr=2019-10-12, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1769389091727, onlineIssueDateStr=2026-01-26, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1769389091727, creator=13701087609, updateTime=1769389091727, updator=13701087609, issue=Issue{id=1222469705873481976, tenantId=1146029695717560320, journalId=1189982191388893191, year='2019', volume='54', issue='10', pageStart='1711', pageEnd='1880', issueExtLink='null', onlineDate='null', pubDate='1570809600000', pubDateStr='2019-10-12', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1769389090269, creator='13701087609', updateTime=1769389551199, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1222471639254683958, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1222469705873481976, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1222471639254683959, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1222469705873481976, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1845, endPage=1850, ext={EN=ArticleExt(id=1222469712475316647, articleId=1222469711988777366, tenantId=1146029695717560320, journalId=1189982191388893191, language=EN, title=DEPTOR improves cisplatin chemosensitivity in esophageal squamous cell carcinoma cells by inducing Caspase-1-mediated pyroptosis, columnId=1190335348761793317, journalTitle=Acta Pharmaceutica Sinica, columnName=Original Articles, runingTitle=null, highlight=null, articleAbstract=

Chemotherapy resistance is the main cause of poor prognosis in patients with advanced esophageal squamous cell carcinoma (ESCC). Pyroptosis is one of the anti-tumor mechanisms by chemotherapy drugs. Studies have shown that DEP-domain containing mTOR-interacting protein (DEPTOR) is correlated with sorafenib and gefitnib resistance, which is discovered as a naturally negative regulator of mammalian/mechanistic target of rapamicin (mTOR). In this study, DEPTOR knockdown (shDEPTOR) lentivirus was used to establish the stable DEPTOR knockdown ESCC cell lines. The results showed that knockdown of DEPTOR reduced chemosensitivity to cisplatin in ESCC cells in vitro. The lower expression of DEPTOR caused less extensive morphological characteristics of pyroptosis than that was observed in sh-con cells with the treatment of cisplain. Further studies showed that knockdown of DEPTOR induced downregulation of Caspase-1 expression and reduction of Caspase-1 activation, thereby inhibiting the activation of the classical pathway of pyroptosis. This paper demonstrates that DEPTOR can improve cisplatin chemosensitivity in ESCC cells via inducing Caspase-1-mediated pyroptosis.

, authors=null, authorsList=Jing-jing DUAN, Hui-xin XU, Pu LUO, Wen-jun PAN, Xiao-ying DONG, Hang ZHENG, authorCompany=null, correspAuthors=Hang ZHENG, authorNote=null, correspAuthorsNote=null, copyrightStatement=Copyright ©2019 Acta Pharmaceutica Sinica. All rights reserved., copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1222469713624555981, articleId=1222469711988777366, tenantId=1146029695717560320, journalId=1189982191388893191, language=CN, title=DEPTOR诱导Caspase-1介导的细胞焦亡提高食管鳞癌细胞顺铂化疗敏感性, columnId=1190335348896011050, journalTitle=药学学报, columnName=研究论文, runingTitle=null, highlight=null, articleAbstract=

化疗耐药是导致晚期食管鳞癌（esophageal squamous cell carcinoma，ESCC）患者预后不良的主要原因。细胞焦亡是化疗药物发挥抗肿瘤作用的机制之一。研究表明，包含DEP域的与哺乳类动物雷帕霉素靶蛋白相互作用的蛋白（DEP-domain containing mTOR-interacting protein，DEPTOR）作为雷帕霉素靶蛋白（mammalian/mechanistic target of rapamycin，mTOR）的内源性抑制蛋白，与索拉非尼、吉非替尼耐药有关。本研究利用DEPTOR敲减（shDEPTOR）慢病毒载体，建立DEPTOR敲减的食管鳞癌细胞稳定表达株。结果表明：在DEPTOR敲减食管鳞癌细胞中，细胞对顺铂的敏感性降低。在顺铂刺激下，DEPTOR敲减的细胞发生典型细胞焦亡形态学的改变较对照组减少。进一步研究表明：DEPTOR表达的减少导致Caspase-1蛋白表达的降低及活化减少，从而抑制细胞焦亡经典途径的激活。本文结果表明，DEPTOR可以通过增加Caspase-1介导的细胞焦亡，提高食管鳞癌细胞对顺铂的敏感性。

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