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Research Article

KLF4 mediates the effect of 5-ASA on the β-catenin pathway in colon cancer cells

Sandra Parenti, Lucia Montorsi, Sebastian Fantini, Fabiana Mammoli, Claudia Gemelli, Claudio Giacinto Atene, Lorena Losi, Chiara Frassineti, Bruno Calabretta, Enrico Tagliafico, Sergio Ferrari, Tommaso Zanocco-Marani and Alexis Grande
Sandra Parenti
Department of Life Sciences, University of Modena and Reggio Emilia
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Lucia Montorsi
Department of Life Sciences, University of Modena and Reggio Emilia
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Sebastian Fantini
Department of Life Sciences, University of Modena and Reggio Emilia
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Fabiana Mammoli
Department of Life Sciences, University of Modena and Reggio Emilia
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Claudia Gemelli
Fondazione Democenter-Sipe, 2Science and Technology Park for Medicine, Mirandola, Modena
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Claudio Giacinto Atene
Department of Life Sciences, University of Modena and Reggio Emilia
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Lorena Losi
Department of Pathology, University of Modena and Reggio Emilia
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Chiara Frassineti
Department of Biomedical, Metabolic and Neuro Sciences, University of Modena and Reggio Emilia
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Bruno Calabretta
Department of Cancer Biology, Sidney Kimmel Cancer Center, Thomas Jefferson University
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Enrico Tagliafico
Center for Genome Research, University of Modena and Reggio Emilia
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Sergio Ferrari
Department of Biomedical Sciences, Biological Chemistry Section, University of Modena and Reggio Emilia
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Tommaso Zanocco-Marani
Department of Life Sciences, University of Modena and Reggio Emilia
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Alexis Grande
Department of Life Sciences, University of Modena and Reggio Emilia
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  • For correspondence: alexis.grande@unimore.it
DOI: 10.1158/1940-6207.CAPR-17-0382
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Abstract

Mesalazine (5-ASA) is an aminosalicylate anti-inflammatory drug capable of inducing μ-protocadherin, a protein expressed by colorectal epithelial cells which is downregulated upon malignant transformation. Treatment with 5-ASA restores μ-protocadherin expression and promotes the sequestration of β-catenin to the plasma membrane. Here we show that 5-ASA-induced μ-protocadherin expression is directly regulated by the KLF4 transcription factor. In addition, we suggest the existence of a dual mechanism whereby 5-ASA-mediated β-catenin inhibition is caused by μ-protocadherin-dependent sequestration of β-catenin to the plasma membrane and by the direct binding of KLF4 to β-catenin. In addition, we found that 5-ASA treatment suppresses the expression of miR-130a and miR-135b, which target KLF4 mRNA, raising the possibility that this mechanism is involved in the increased expression of KLF4 induced by 5-ASA.

  • Received November 27, 2017.
  • Revision received April 10, 2018.
  • Accepted May 16, 2018.
  • Copyright ©2018, American Association for Cancer Research.

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Published OnlineFirst May 24, 2018
doi: 10.1158/1940-6207.CAPR-17-0382

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KLF4 mediates the effect of 5-ASA on the β-catenin pathway in colon cancer cells
Sandra Parenti, Lucia Montorsi, Sebastian Fantini, Fabiana Mammoli, Claudia Gemelli, Claudio Giacinto Atene, Lorena Losi, Chiara Frassineti, Bruno Calabretta, Enrico Tagliafico, Sergio Ferrari, Tommaso Zanocco-Marani and Alexis Grande
Cancer Prev Res May 24 2018 DOI: 10.1158/1940-6207.CAPR-17-0382

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KLF4 mediates the effect of 5-ASA on the β-catenin pathway in colon cancer cells
Sandra Parenti, Lucia Montorsi, Sebastian Fantini, Fabiana Mammoli, Claudia Gemelli, Claudio Giacinto Atene, Lorena Losi, Chiara Frassineti, Bruno Calabretta, Enrico Tagliafico, Sergio Ferrari, Tommaso Zanocco-Marani and Alexis Grande
Cancer Prev Res May 24 2018 DOI: 10.1158/1940-6207.CAPR-17-0382
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Cancer Prevention Research
eISSN: 1940-6215
ISSN: 1940-6207

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