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Sci Rep. 2018 Aug 7;8(1):11797. doi: 10.1038/s41598-018-30307-x.

The atypical cyclin CNTD2 promotes colon cancer cell proliferation and migration.

Author information

1
Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya, Barcelona, Spain.
2
Pathology Department, Hospital Universitari General de Catalunya, Sant Cugat del Vallès, Barcelona, Spain.
3
Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, USA.
4
Department of Pathology, University Hospital of Bellvitge, Bellvitge Biomedical Research Institute (IDIBELL), CIBERONC, L'Hospitalet del Llobregat, Barcelona, Spain.
5
Xenopat S.L., Business Bioincubator, Bellvitge Health Science Campus, Barcelona, Spain.
6
Chemoresistance and Predictive Factors Group, Program Against Cancer Therapeutic Resistance (ProCURE), Catalan Institute of Oncology (ICO) Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet del Llobregat, Barcelona, Spain.
7
Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya, Barcelona, Spain. mpontecardosoribeiro@uic.es.
8
Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya, Barcelona, Spain. jclotet@uic.es.

Abstract

Colorectal cancer (CRC) is one of the most common cancers worldwide, with 8-10% of these tumours presenting a BRAF (V600E) mutation. Cyclins are known oncogenes deregulated in many cancers, but the role of the new subfamily of atypical cyclins remains elusive. Here we have performed a systematic analysis of the protein expression levels of eight atypical cyclins in human CRC tumours and several cell lines, and found that CNTD2 is significantly upregulated in CRC tissue compared to the adjacent normal one. CNTD2 overexpression in CRC cell lines increases their proliferation capacity and migration, as well as spheroid formation capacity and anchorage-independent growth. Moreover, CNTD2 increases tumour growth in vivo on xenograft models of CRC with wild-type BRAF. Accordingly, CNTD2 downregulation significantly diminished the proliferation of wild-type BRAF CRC cells, suggesting that CNTD2 may represent a new prognostic factor and a promising drug target in the management of CRC.

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