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Berlin, Christopher [Author]; Schüle, Roland [Author] ; Hecht, Andreas [Other]; Schüle, Roland [Degree supervisor] Universitätsklinikum Freiburg Zentrale Klinische Forschung, Klinik für Allgemein- und Viszeralchirurgie, Albert-Ludwigs-Universität Freiburg Fakultät für Biologie

KMT9 controls stemness and growth of colorectal cancer

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  • Media type: E-Book
  • Title: KMT9 controls stemness and growth of colorectal cancer
  • Contributor: Berlin, Christopher [Verfasser]; Schüle, Roland [Verfasser]; Hecht, Andreas [Sonstige]; Schüle, Roland [Akademischer Betreuer]
  • Corporation: Universitätsklinikum Freiburg, Zentrale Klinische Forschung ; Klinik für Allgemein- und Viszeralchirurgie ; Albert-Ludwigs-Universität Freiburg, Fakultät für Biologie
  • imprint: Freiburg: Universität, 2022
  • Extent: Online-Ressource
  • Language: English
  • DOI: 10.6094/UNIFR/223790
  • Identifier:
  • Keywords: Dickdarmkrebs ; Histone ; Epigenetik ; Therapie ; (local)doctoralThesis
  • Origination:
  • University thesis: Dissertation, Universität Freiburg, 2022
  • Footnote:
  • Description: Abstract: According to data from the world health organisation (WHO), colorectal cancer (CRC) is responsible for more than 900,000 deaths per year and thereby is the second- and third most common tumour entity in women and men worldwide. Whereas low tumour stages are well treatable by surgery, patients with higher tumour stages are in need of neoadjuvant or adjuvant systemic therapeutic approaches. Treatment failure and tumour relapse represent a common issue in clinical reality and both problems are being attributed to therapy resistance and survival of cancer stem cells (CSC).<br>In this project, we investigated the mode of action of lysine methyltransferase 9 (KMT9), an obligate heterodimer composed of KMT9a and KMT9b which can monomethylate histone H4 at lysine 12 (H4K12me1) in CRC. Both subunits of KMT9 show elevated expression levels in CRC and colocalize with the methyl mark H4K12me1 at the promoter region of target genes which are involved in the regulation of proliferation. Depletion of KMT9a reduces inflammation-dependent colorectal tumourigenesis in mice and prevents the growth of murine as well as human patient-derived tumour organoids (PDO). Additionally, ablation of KMT9a reduces CSC function and survival by induction of apoptosis. Together, obtained data from this project bring KMT9 into play as fundamental regulator of colorectal carcinogenesis and identifies KMT9 as a promising therapeutic target for the systemic treatment of CRC
  • Access State: Restricted Access | Information to licenced electronic resources of the SLUB