000141315 001__ 141315
000141315 005__ 20240303003516.0
000141315 0247_ $$2doi$$a10.3892/ijo.2018.4616
000141315 0247_ $$2pmid$$apmid:30387838
000141315 0247_ $$2ISSN$$a1019-6439
000141315 0247_ $$2ISSN$$a1791-2423
000141315 0247_ $$2altmetric$$aaltmetric:152887987
000141315 037__ $$aDKFZ-2018-01834
000141315 041__ $$aeng
000141315 082__ $$a610
000141315 1001_ $$aAbukiwan, Alia$$b0
000141315 245__ $$aDexamethasone-induced inhibition of miR-132 via methylation promotes TGF-β-driven progression of pancreatic cancer.
000141315 260__ $$aAthens$$bSpandidos Publ.$$c2019
000141315 3367_ $$2DRIVER$$aarticle
000141315 3367_ $$2DataCite$$aOutput Types/Journal article
000141315 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1551177036_32589
000141315 3367_ $$2BibTeX$$aARTICLE
000141315 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000141315 3367_ $$00$$2EndNote$$aJournal Article
000141315 520__ $$aGlucocorticoids (GCs) such as dexamethasone (DEX) are administered as cancer co‑treatment for palliative purposes due to their pro‑apoptotic effects in lymphoid cancer and limited side effects associated with cancer growth and chemotherapy. However, there is emerging evidence that GCs induce therapy resistance in most epithelial tumors. Our recent data reveal that DEX promotes the progression of pancreatic ductal adenocarcinoma (PDA). In the present study, we examined 1 primary and 2 established PDA cell lines, and 35 PDA tissues from patients who had received (n=14) or not received (n=21) GCs prior to surgery. Through microRNA microarray analysis, in silico, and RT‑qPCR analyses, we identified 268 microRNAs differentially expressed between DEX‑treated and untreated cells. With a focus on cancer progression, we selected miR‑132 and its target gene, transforming growth factor-β2 (TGF‑β2), as top candidates. miR‑132 mimics directly bound to the 3' untranslated region (3'UTR) of a TGF‑β2 luciferase construct and enhanced expression, as shown by increased luciferase activity. By contrast, DEX inhibited miR‑132 expression via promoter methylation. miR‑132 mimics also reduced DEX‑induced clonogenicity, migration and expression of vimentin and E‑cadherin in vitro and in tumor xenografts. In patients, GC intake prior to surgery enhanced global hypermethylation and expression of TGF‑β2 in tissues; expression of miR‑132 was detected but could not be quantified. Our results demonstrate that DEX‑mediated inhibition of miR‑132 is a key mediator in the progression of pancreatic cancer, and the findings provide a foundation for miRNA‑based therapies.
000141315 536__ $$0G:(DE-HGF)POF3-313$$a313 - Cancer risk factors and prevention (POF3-313)$$cPOF3-313$$fPOF III$$x0
000141315 588__ $$aDataset connected to CrossRef, PubMed,
000141315 7001_ $$aNwaeburu, Clifford C$$b1
000141315 7001_ $$aBauer, Nathalie$$b2
000141315 7001_ $$aZhao, Zhefu$$b3
000141315 7001_ $$aLiu, Li$$b4
000141315 7001_ $$aGladkich, Jury$$b5
000141315 7001_ $$aGross, Wolfgang$$b6
000141315 7001_ $$0P:(DE-He78)e15dfa1260625c69d6690a197392a994$$aBenner, Axel$$b7$$udkfz
000141315 7001_ $$aStrobel, Oliver$$b8
000141315 7001_ $$aFellenberg, Jörg$$b9
000141315 7001_ $$aHerr, Ingrid$$b10
000141315 773__ $$0PERI:(DE-600)2079608-0$$a10.3892/ijo.2018.4616$$n1$$p53-64$$tInternational journal of oncology$$v54$$x1791-2423$$y2019
000141315 909CO $$ooai:inrepo02.dkfz.de:141315$$pVDB
000141315 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline
000141315 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database
000141315 915__ $$0StatID:(DE-HGF)0320$$2StatID$$aDBCoverage$$bPubMed Central
000141315 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bINT J ONCOL : 2017
000141315 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS
000141315 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List
000141315 915__ $$0StatID:(DE-HGF)0110$$2StatID$$aWoS$$bScience Citation Index
000141315 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection
000141315 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded
000141315 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences
000141315 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews
000141315 915__ $$0StatID:(DE-HGF)9900$$2StatID$$aIF < 5
000141315 9141_ $$y2019
000141315 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)e15dfa1260625c69d6690a197392a994$$aDeutsches Krebsforschungszentrum$$b7$$kDKFZ
000141315 9131_ $$0G:(DE-HGF)POF3-313$$1G:(DE-HGF)POF3-310$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vCancer risk factors and prevention$$x0
000141315 9201_ $$0I:(DE-He78)C060-20160331$$kC060$$lBiostatistik$$x0
000141315 980__ $$ajournal
000141315 980__ $$aVDB
000141315 980__ $$aI:(DE-He78)C060-20160331
000141315 980__ $$aUNRESTRICTED