ArticleScientific reports2017
A systematic analysis of orphan cyclins reveals CNTD2 as a new oncogenic driver in lung cancer.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Acquired resistance to immunotherapy and chemoradiation in MYC amplified head and neck cancer.NPJ precision oncology · 2024Article
- CDK6 is activated by the atypical cyclin I to promote E2F-mediated gene expression and cancer cell proliferation.Molecular oncology · 2023Article
- DNA damage repair gene signature model for predicting prognosis and chemotherapy outcomes in lung squamous cell carcinoma.BMC cancer · 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
- Atypical cyclins: the extended family portrait.Cellular and molecular life sciences : CMLS · 2020Review
- The atypical cyclin CNTD2 promotes colon cancer cell proliferation and migration.Scientific reports · 2018Article
- A universal mammalian vaccine cell line substrate.PloS one · 2017Article
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
As lung cancer has increased to the most common cause of cancer death worldwide, prognostic biomarkers and effective targeted treatments remain lacking despite advances based on patients' stratification. Multiple core cyclins, best known as drivers of cell proliferation, are commonly deregulated in lung cancer where they may serve as oncogenes. The recent expansion of the cyclin family raises the question whether new members might play oncogenic roles as well. Here, we investigated the protein levels of eight atypical cyclins in lung cancer cell lines and formalin-fixed and paraffin-embedded (FFPE) human tumors, as well as their functional role in lung cancer cells. Of the new cyclins evaluated, CNTD2 was significantly overexpressed in lung cancer compared to adjacent normal tissue, and exhibited a predominant nuclear location. CNTD2 overexpression increased lung cancer cell viability, Ki-67 intensity and clonogenicity and promoted lung cancer cell migration. Accordingly, CNTD2 enhanced tumor growth in vivo on A549 xenograft models. Finally, the analysis of gene expression data revealed a high correlation between elevated levels of CNTD2 and decreased overall survival in lung cancer patients. Our results reveal CNTD2 as a new oncogenic driver in lung cancer, suggesting value as a prognostic biomarker and therapeutic target in this disease.
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