ArticleScientific reports2018
The atypical cyclin CNTD2 promotes colon cancer cell proliferation and migration.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Charting the regulatory landscape of TP53 on transposable elements in cancer.Genome research · 2025Article
- Acquired resistance to immunotherapy and chemoradiation in MYC amplified head and neck cancer.NPJ precision oncology · 2024Article
- Integrative molecular analysis of combined small-cell lung carcinomas identifies major subtypes with different therapeutic opportunities.ESMO open · 2022Article
- Atypical cyclin P regulates cancer cell stemness through activation of the WNT pathway.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- Screening and Identification of Key Common and Specific Genes and Their Prognostic Roles in Different Molecular Subtypes of Breast Cancer.Frontiers in molecular biosciences · 2021Article
- Enhanced Expression ofFrontiers in genetics · 2021Article
- Network-based identification of biomarkers for colon adenocarcinoma.BMC cancer · 2020Article
- Atypical cyclins: the extended family portrait.Cellular and molecular life sciences : CMLS · 2020Review
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
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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Registered trials
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