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@ARTICLE{Rose:892293,
      author       = {Rose, Michael and Noetzel, Erik and Kistermann, Jennifer
                      and Eschenbruch, Julian and Rushrush, Sandra and Gan, Lin
                      and Knüchel, Ruth and Gaisa, Nadine T. and Dahl, Edgar},
      title        = {{T}he {ECM} {M}odulator {ITIH}5 {A}ffects {C}ell
                      {A}dhesion, {M}otility and {C}hemotherapeutic {R}esponse of
                      {B}asal/{S}quamous-{L}ike ({BASQ}) {B}ladder {C}ancer
                      {C}ells},
      journal      = {Cells},
      volume       = {10},
      number       = {5},
      issn         = {2073-4409},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {FZJ-2021-02002},
      pages        = {1038 -},
      year         = {2021},
      abstract     = {This study aims at characterizing the role of the putative
                      tumor suppressor ITIH5 in basal-type bladder cancers (BLCA).
                      By sub-classifying TCGA BLCA data, we revealed predominant
                      loss of ITIH5 expression in the basal/squamous-like (BASQ)
                      subtype. ITIH5 expression inversely correlated with
                      basal-type makers such as KRT6A and CD44. Interestingly,
                      Kaplan–Meier analyses showed longer recurrence-free
                      survival in combination with strong CD44 expression, which
                      is thought to mediate ITIH-hyaluronan (HA) binding
                      functions. In vitro, stable ITIH5 overexpression in two
                      basal-type BLCA cell lines showing differential CD44
                      expression levels, i.e., with (SCaBER) and without squamous
                      features (HT1376), demonstrated clear inhibition of cell and
                      colony growth of BASQ-type SCaBER cells. ITIH5 further
                      enhanced HA-associated cell-matrix attachment, indicated by
                      altered size and number of focal adhesion sites resulting in
                      reduced cell migration capacities. Transcriptomic analyses
                      revealed enrichment of pathways and processes involved in
                      ECM organization, differentiation and cell signaling.
                      Finally, we provide evidence that ITIH5 increase sensitivity
                      of SCaBER cells to chemotherapeutical agents (cisplatin and
                      gemcitabine), whereas responsiveness of HT1376 cells was not
                      affected by ITIH5 expression. Thus, we gain further insights
                      into the putative role of ITIH5 as tumor suppressor
                      highlighting an impact on drug response potentially via the
                      HA-CD44 axis in BASQ-type BLCA},
      cin          = {IBI-2},
      ddc          = {570},
      cid          = {I:(DE-Juel1)IBI-2-20200312},
      pnm          = {524 - Molecular and Cellular Information Processing
                      (POF4-524)},
      pid          = {G:(DE-HGF)POF4-524},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {33924987},
      UT           = {WOS:000654663800001},
      doi          = {10.3390/cells10051038},
      url          = {https://juser.fz-juelich.de/record/892293},
}