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@ARTICLE{Even:143038,
      author       = {I. Even$^*$ and S. Reidenbach$^*$ and T. Schlechter$^*$ and
                      N. Berns and R. Herold$^*$ and W. Roth$^*$ and D. Krunic$^*$
                      and V. Riechmann and I. Hofmann$^*$},
      title        = {{DLIC}1, but not {DLIC}2, is upregulated in colon cancer
                      and this contributes to proliferative overgrowth and
                      migratory characteristics of cancer cells.},
      journal      = {The FEBS journal},
      volume       = {286},
      number       = {4},
      issn         = {1742-464X},
      address      = {Oxford [u.a.]},
      publisher    = {Wiley-Blackwell},
      reportid     = {DKFZ-2019-00657},
      pages        = {803 - 820},
      year         = {2019},
      note         = {DKFZ ZMBH Alliance},
      abstract     = {Cytoplasmic dynein-1 is a large minus-end-directed
                      microtubule motor complex involved in membrane trafficking,
                      organelle positioning, and microtubule organization. The
                      roles of dynein light intermediate chains (DLICs; DLIC1 and
                      DLIC2) within the complex are, however, still largely
                      undefined. In this study, we investigated the possible roles
                      of DLICs in epithelial homeostasis and colon cancer
                      development. Mutant clonal analysis of Drosophila Dlic in
                      the follicular epithelium of Drosophila ovary showed defects
                      in nuclear positioning, epithelial integrity, and apical
                      cell polarity. Consistently, knockdown of human DLIC1 and
                      DLIC2 in colon carcinoma cells resulted in damaged
                      epithelial organization, disturbed lumen formation, and
                      impaired apical polarity establishment in three-dimensional
                      cell culture. Depletion of DLIC1 and DLIC2 led to reduced
                      proliferation, enhanced apoptosis rates, disrupted mitotic
                      spindle assembly, and induction of G2/M arrest in cell cycle
                      progression. Moreover, reduced levels of DLIC1 in contrast
                      to DLIC2 impaired the migratory ability. On the other hand,
                      immunohistochemical examination of human colorectal tissue
                      samples and further colorectal cancer dataset analysis
                      showed a significant upregulation for DLIC1 in tumors,
                      whereas DLIC2 expression was unchanged. In addition, the
                      overexpression of DLIC1 caused increased proliferation,
                      decreased apoptosis and enhanced migration, whereas DLIC2
                      overexpression did not result in any significant changes.
                      Together, these results indicate that DLIC1 and DLIC2
                      contribute to the establishment and maintenance of
                      epithelial homeostasis. Furthermore, these findings present
                      the first evidence that DLIC1 and DLIC2 have distinct roles
                      in colon cancer development and that DLIC1 may contribute to
                      proliferative overgrowth and migratory characteristics.},
      cin          = {A190 / G150 / W210},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331 / I:(DE-He78)G150-20160331 /
                      I:(DE-He78)W210-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30657258},
      doi          = {10.1111/febs.14755},
      url          = {https://inrepo02.dkfz.de/record/143038},
}