% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Shukla:127516,
      author       = {K. Shukla$^*$ and A. K. Sharma$^*$ and A. Ward$^*$ and R.
                      Will$^*$ and T. Hielscher$^*$ and A. Balwierz$^*$ and C.
                      Breunig$^*$ and E. Münstermann$^*$ and R. König$^*$ and I.
                      Keklikoglou$^*$ and S. Wiemann$^*$},
      title        = {{M}icro{RNA}-30c-2-3p negatively regulates {NF}-κ{B}
                      signaling and cell cycle progression through downregulation
                      of {TRADD} and {CCNE}1 in breast cancer.},
      journal      = {Molecular oncology},
      volume       = {9},
      number       = {6},
      issn         = {1574-7891},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2017-03539},
      pages        = {1106 - 1119},
      year         = {2015},
      abstract     = {Nuclear Factor kappa B (NF-κB) signaling is frequently
                      deregulated in a variety of cancers and is constitutively
                      active in estrogen receptor negative (ER-) breast cancer
                      subtypes. These molecular subtypes of breast cancer are
                      associated with poor overall survival. We focused on
                      mechanisms of NF-κB regulation by microRNAs (miRNAs), which
                      regulate eukaryotic gene expression at the
                      post-transcriptional level. In a previous genome-wide miRNA
                      screen, we had identified miR-30c-2-3p as one of the
                      strongest negative regulators of NF-κB signaling. Here we
                      have uncovered the underlying molecular mechanisms and its
                      consequences in breast cancer. In vitro results show that
                      miR-30c-2-3p directly targets both TNFRSF1A-associated via
                      death domain (TRADD), an adaptor protein of the TNFR/NF-κB
                      signaling pathway, and the cell cycle protein Cyclin E1
                      (CCNE1). Ectopic expression of miR-30c-2-3p downregulated
                      essential cytokines IL8, IL6, CXCL1, and reduced cell
                      proliferation as well as invasion in MDA-MB-231 breast
                      cancer cells. RNA interference (RNAi) induced silencing of
                      TRADD phenocopied the effects on invasion and cytokine
                      expression caused by miR-30c-2-3p, while inhibition of CCNE1
                      phenocopied the effects on cell proliferation. We further
                      confirmed the tumor suppressive role of this miRNA using a
                      dataset of 781 breast tumors, where higher expression was
                      associated with better survival in breast cancer patients.
                      In summary we have elucidated the mechanism by which
                      miR-30c-2-3p negatively regulates NF-κB signaling and cell
                      cycle progression in breast cancer.},
      keywords     = {CCNE1 protein, human (NLM Chemicals) / Cyclin E (NLM
                      Chemicals) / MIRN30 microRNA, human (NLM Chemicals) /
                      MicroRNAs (NLM Chemicals) / NF-kappa B (NLM Chemicals) /
                      Oncogene Proteins (NLM Chemicals) / RNA, Neoplasm (NLM
                      Chemicals) / TNF Receptor-Associated Death Domain Protein
                      (NLM Chemicals)},
      cin          = {B050 / B080 / W110 / C060},
      ddc          = {610},
      cid          = {I:(DE-He78)B050-20160331 / I:(DE-He78)B080-20160331 /
                      I:(DE-He78)W110-20160331 / I:(DE-He78)C060-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25732226},
      pmc          = {pmc:PMC5528752},
      doi          = {10.1016/j.molonc.2015.01.008},
      url          = {https://inrepo02.dkfz.de/record/127516},
}