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@ARTICLE{Abukiwan:141315,
      author       = {A. Abukiwan and C. C. Nwaeburu and N. Bauer and Z. Zhao and
                      L. Liu and J. Gladkich and W. Gross and A. Benner$^*$ and O.
                      Strobel and J. Fellenberg and I. Herr},
      title        = {{D}examethasone-induced inhibition of mi{R}-132 via
                      methylation promotes {TGF}-β-driven progression of
                      pancreatic cancer.},
      journal      = {International journal of oncology},
      volume       = {54},
      number       = {1},
      issn         = {1791-2423},
      address      = {Athens},
      publisher    = {Spandidos Publ.},
      reportid     = {DKFZ-2018-01834},
      pages        = {53-64},
      year         = {2019},
      abstract     = {Glucocorticoids (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.},
      cin          = {C060},
      ddc          = {610},
      cid          = {I:(DE-He78)C060-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30387838},
      doi          = {10.3892/ijo.2018.4616},
      url          = {https://inrepo02.dkfz.de/record/141315},
}