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10.14348/molcells.2016.0150

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suck abstract from ncbi


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pmid27432190
      Mol+Cells 2016 ; 39 (8 ): 625-30
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  • Transforming Growth Factor-?-Induced RBFOX3 Inhibition Promotes Epithelial-Mesenchymal Transition of Lung Cancer Cells #MMPMID27432190
  • Kim YE ; Kim JO ; Park KS ; Won M ; Kim KE ; Kim KK
  • Mol Cells 2016[Aug]; 39 (8 ): 625-30 PMID27432190 show ga
  • The RNA-binding protein Rbfox3 is a well-known splicing regulator that is used as a marker for post-mitotic neurons in various vertebrate species. Although recent studies indicate a variable expression of Rbfox3 in non-neuronal tissues, including lung tissue, its cellular function in lung cancer remains largely unknown. Here, we report that the number of RBFOX3-positive cells in tumorous lung tissue is lower than that in normal lung tissue. As the transforming growth factor-? (TGF-?) signaling pathway is important in cancer progression, we investigated its role in RBFOX3 expression in A549 lung adenocarcinoma cells. TGF-?1 treatment inhibited RBFOX3 expression at the transcriptional level. Further, RBFOX3 depletion led to a change in the expression levels of a subset of proteins related to epithelial-mesenchymal transition (EMT), such as E-cadherin and Claudin-1, during TGF-?1-induced EMT. In immunofluorescence microscopic analysis, mesenchymal morphology was more prominent in RBFOX3-depleted cells than in control cells. These findings show that TGF-?-induced RBFOX3 inhibition plays an important role in EMT and propose a novel role for RBFOX3 in cancer progression.
  • |*Epithelial-Mesenchymal Transition/genetics [MESH]
  • |Adenocarcinoma of Lung [MESH]
  • |Adenocarcinoma/genetics/*metabolism [MESH]
  • |Antigens, Nuclear/genetics/*metabolism [MESH]
  • |Cadherins/metabolism [MESH]
  • |Carcinogenesis/genetics [MESH]
  • |Cell Line, Tumor [MESH]
  • |Claudin-1/metabolism [MESH]
  • |Gene Expression Regulation, Neoplastic [MESH]
  • |Humans [MESH]
  • |Lung Neoplasms/genetics/*metabolism [MESH]
  • |Nerve Tissue Proteins/genetics/*metabolism [MESH]
  • |RNA Splicing/genetics [MESH]
  • |RNA, Small Interfering/genetics [MESH]
  • |Respiratory Mucosa/*metabolism/pathology [MESH]
  • |Signal Transduction [MESH]


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