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@ARTICLE{Tagscherer:130642,
      author       = {K. Tagscherer$^*$ and A. Fassl$^*$ and T. Sinkovic$^*$ and
                      J. Richter$^*$ and S. Schecher$^*$ and S.
                      Macher-Goeppinger$^*$ and W. Roth$^*$},
      title        = {{M}icro{RNA}-210 induces apoptosis in colorectal cancer via
                      induction of reactive oxygen.},
      journal      = {Cancer cell international},
      volume       = {16},
      number       = {1},
      issn         = {1475-2867},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DKFZ-2017-05720},
      pages        = {42},
      year         = {2016},
      abstract     = {Deregulation of miRNA-210 is a common event in several
                      types of cancer. However, increased expression levels in the
                      cancer tissue have been associated with both poor and good
                      prognosis of patients. Similarly, the function of miR-210
                      with regard to cell growth and apoptosis is still
                      controversial.Overexpression of miR-210 was performed in
                      HCT116, SW480 and SW707 colorectal cancer (CRC) cell lines.
                      Functional effects of a modulated miR-210 expression were
                      analyzed with regard to proliferation, clonogenicity, cell
                      cycle distribution, reactive oxygen species (ROS)
                      generation, and apoptosis. Furthermore, quantitative real
                      time (RT)-PCR and immunoblot analyses were performed to
                      investigate signaling pathways affected by miR-210.We show
                      that in CRC cells miR-210 inhibits clonogenicity and
                      proliferation which was accompanied by an accumulation of
                      cells in the G2/M phase of the cell cycle. Additionally,
                      overexpression of miR-210 results in an increase of ROS
                      generation. Moreover, miR-210 mediated the induction of
                      apoptosis which was associated with an upregulation of
                      pro-apoptotic Bim expression and enhanced processing of
                      Caspase 2. Importantly, inhibition of ROS generation rescued
                      cells from miR-210-induced apoptosis.Taken together, miR-210
                      induces apoptosis in CRC cells via a ROS-dependent
                      mechanism.},
      cin          = {G150},
      ddc          = {610},
      cid          = {I:(DE-He78)G150-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27293381},
      pmc          = {pmc:PMC4901463},
      doi          = {10.1186/s12935-016-0321-6},
      url          = {https://inrepo02.dkfz.de/record/130642},
}