Polycomb group ring finger protein 6 suppresses Myc-induced lymphomagenesis

Author:

Tanaskovic Nina1ORCID,Dalsass Mattia1ORCID,Filipuzzi Marco1,Ceccotti Giorgia1,Verrecchia Alessandro1ORCID,Nicoli Paola1,Doni Mirko1ORCID,Olivero Daniela2ORCID,Pasini Diego13,Koseki Haruhiko45ORCID,Sabò Arianna1,Bisso Andrea1ORCID,Amati Bruno1ORCID

Affiliation:

1. European Institute of Oncology (IEO) - IRCCS, Milan, Italy

2. Laboratorio Analisi Veterinarie BiEsseA, A Company of Scil Animal Care Company Srl, Milan, Italy

3. Department of Health Sciences, University of Milan, Milan, Italy

4. Laboratory of Developmental Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan

5. Cellular and Molecular Medicine, Advanced Research Departments, Graduate School of Medicine, Chiba University, Chiba, Japan

Abstract

Max is an obligate dimerization partner for the Myc transcription factors and for several repressors, such as Mnt, Mxd1-4, and Mga, collectively thought to antagonize Myc function in transcription and oncogenesis. Mga, in particular, is part of the variant Polycomb group repressive complex PRC1.6. Here, we show that ablation of the distinct PRC1.6 subunit Pcgf6–but not Mga–accelerates Myc-induced lymphomagenesis in Eµ-myc transgenic mice. Unexpectedly, however, Pcgf6 loss shows no significant impact on transcriptional profiles, in neither pre-tumoral B-cells, nor lymphomas. Altogether, these data unravel an unforeseen, Mga- and PRC1.6-independent tumor suppressor activity of Pcgf6.

Funder

Italian Health Ministry

Italian Association for Cancer Research

Ministry of Education, Culture, Sports, Science and Technology of Japan

Publisher

Life Science Alliance, LLC

Subject

Health, Toxicology and Mutagenesis,Plant Science,Biochemistry, Genetics and Molecular Biology (miscellaneous),Ecology

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