Advertisement

Methods for In Vivo Functional Studies of Chromatin-Modifying Enzymes in Early Steps of Colon Carcinogenesis

  • Martine Chevillard-Briet
  • Fabrice Escaffit
Protocol
Part of the Methods in Molecular Biology book series (MIMB, volume 1765)

Abstract

Since chromatin-modifying enzymes are involved in most processes needing to access the DNA fiber such as transcription, replication or DNA repair, their involvement in the regulation of gene expression in numerous physiopathological contexts is widely studied. Most of these enzymes are essential for cell growth and survival due to their pleiotropic roles and studying their impact in vivo on organ development or tissue physiopathology is challenging. In this chapter, we describe a chemically-mediated method to induce colorectal carcinogenesis that we have used to identify in vivo the role of two chromatin modifying enzymes belonging to the same multimolecular complex, the histone acetyltransferase Tip60 and the histone variant-incorporating ATPase p400.

Key words

Chromatin Aberrant crypt foci Adenomas Colon cancer Mouse models Chemically induced carcinogenesis Azoxymethane (AOM) Dextran sodium sulfate (DSS) Wnt pathway 

Notes

Acknowledgments

We thank Pr Denis Corpet for teaching us the AOM injections and ACF analysis.

The original work described in this chapter [2] was supported by the Ligue Nationale Contre le Cancer as an “Équipe labellisée,” by the Fondation of the Association pour la Recherche contre le Cancer and by the Fondation de France.

References

  1. 1.
    Fullgrabe J, Kavanagh E, Joseph B (2011) Histone onco-modifications. Oncogene 30:3391–3403CrossRefPubMedGoogle Scholar
  2. 2.
    Chevillard-Briet M, Quaranta M, Grezy A, Mattera L, Courilleau C, Philippe M et al (2014) Interplay between chromatin-modifying enzymes controls colon cancer progression through Wnt signaling. Hum Mol Genet 23:2120–2131CrossRefPubMedGoogle Scholar
  3. 3.
    Parnaud G, Tache S, Peiffer G, Corpet DE (1999) Polyethylene-glycol suppresses colon cancer and causes dose-dependent regression of azoxymethane-induced aberrant crypt foci in rats. Cancer Res 59:5143–5147PubMedGoogle Scholar
  4. 4.
    Tanaka T, Kohno H, Suzuki R, Yamada Y, Sugie S, Mori H (2003) A novel inflammation-related mouse colon carcinogenesis model induced by azoxymethane and dextran sodium sulfate. Cancer Sci 94:965–973CrossRefPubMedGoogle Scholar
  5. 5.
    Pierre FH, Santarelli RL, Allam O, Tache S, Naud N, Gueraud F et al (2010) Freeze-dried ham promotes azoxymethane-induced mucin-depleted foci and aberrant crypt foci in rat colon. Nutr Cancer 62:567–573CrossRefPubMedPubMedCentralGoogle Scholar
  6. 6.
    De Robertis M, Massi E, Poeta ML, Carotti S, Morini S, Cecchetelli L et al (2011) The AOM/DSS murine model for the study of colon carcinogenesis: from pathways to diagnosis and therapy studies. J Carcinog 10:9CrossRefPubMedPubMedCentralGoogle Scholar
  7. 7.
    Lopez-Ceron M, Pellise M (2012) Biology and diagnosis of aberrant crypt foci. Color Dis 14:e157–e164CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Laboratoire de Biologie Cellulaire et Moléculaire du Contrôle de la Prolifération (LBCMCP), Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPSToulouseFrance

Personalised recommendations