ArticleCell cycle (Georgetown, Tex.)2014
Functional genomics identify Birc5/survivin as a candidate gene involved in the chronotoxicity of cyclin-dependent kinase inhibitors.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
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- Transcriptome analysis of clock disrupted cancer cells reveals differential alternative splicing of cancer hallmarks genes.NPJ systems biology and applications · 2022Article
- Understanding the significance of biological clock and its impact on cancer incidence.Cancer letters · 2022Review
- Biological Clock and Inflammatory Bowel Disease Review: From the Standpoint of the Intestinal Barrier.Gastroenterology research and practice · 2022Review
- Survivin' Acute Myeloid Leukaemia-A Personalised Target for inv(16) Patients.International journal of molecular sciences · 2021Article
- Melatonin and Cancer: A Polyhedral Network Where the Source Matters.Antioxidants (Basel, Switzerland) · 2021Review
- Survivin expression and impact on head and neck cancer outcomes.Oral oncology · 2021Article
- Survivin at a glance.Journal of cell science · 2019Review
- Circadian rhythms in the pathogenesis of gastrointestinal diseases.World journal of gastroenterology · 2018Article
- Protectiveness of Artesunate Given Prior Ischemic Cerebral Infarction Is Mediated by Increased Autophagy.Frontiers in neurology · 2018Article
- Disruptions in asymmetric centrosome inheritance and WDR62-Aurora kinase B interactions in primary microcephaly.Scientific reports · 2017Article
- Article
- Circadian clocks, epigenetics, and cancer.Current opinion in oncology · 2015Review
- Molecular characterization of an intact p53 pathway subtype in high-grade serous ovarian cancer.PloS one · 2014Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The circadian timing system orchestrates most of mammalian physiology and behavior in synchrony with the external light/dark cycle. This regulation is achieved through endogenous clocks present in virtually all body cells, where they control key cellular processes, including metabolism, transport, and the cell cycle. Consistently, it has been observed in preclinical cancer models that both the efficacy and toxicity of most chemotherapeutic drugs depend on their time of administration. To further explore the molecular basis underlying the link between the circadian timing system and the cellular response to anticancer drugs, we investigated the circadian transcriptome and CDK inhibitor toxicity in colon mucosa cells. We first show here that among 181 circadian transcripts, approximately 30% of them drive the cell cycle in the healthy mouse colon mucosa, with a majority peaking during the early resting phase. The identification of 26 mitotic genes within this cluster further indicated that the transcriptional coordination of mitosis by the circadian clock participates in the gating of cell division in this tissue. Subsequent selective siRNA-mediated silencing of these 26 targets revealed that low expression levels of the mitotic and anti-apoptotic gene Birc5/survivin significantly and specifically increased the sensitivity of colon epithelial cells to CDK inhibitors. By identifying Birc5/survivin as a potential determinant for the circadian modulation of CDK inhibitor toxicity, these data provide a mechanistic basis for the preclinical development of future CDK inhibitor-based chronotherapeutic strategies.
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Registered trials
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