ArticleProceedings of the National Academy of Sciences of the United States of America2011
Circadian clock disruption improves the efficacy of chemotherapy through p73-mediated apoptosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
37 citing papers in PubMed, 62 citations in OpenAlex.
- The interplay between circadian rhythm components and apoptosis in health and disease.Human cell · 2026Review
- Targeting Cryptochromes in Chronic Diseases.Cell biology international · 2025Review
- The Influence of Circadian Rhythms on DNA Damage Repair in Skin Photoaging.International journal of molecular sciences · 2024Review
- Overview on Common Genes Involved in the Onset of Glioma and on the Role of Migraine as Risk Factor: Predictive Biomarkers or Therapeutic Targets?Journal of personalized medicine · 2022Review
- Discovery of a small molecule that selectively destabilizes Cryptochrome 1 and enhances life span in p53 knockout mice.Nature communications · 2022Article
- Genetic Variations within the BovineAnimals : an open access journal from MDPI · 2022Article
- Conservation of dynamic characteristics of transcriptional regulatory elements in periodic biological processes.BMC bioinformatics · 2022Article
- Transcriptional Feedback Loops in the Caprine Circadian Clock System.Frontiers in veterinary science · 2022Article
- The Circadian Clock Gene, Bmal1, Regulates Intestinal Stem Cell Signaling and Represses Tumor Initiation.Cellular and molecular gastroenterology and hepatology · 2021Article
- Thyroid Cancer and Circadian Clock Disruption.Cancers · 2020Review
- Cancer, hear my battle CRY.Journal of pineal research · 2020Review
- Cryptochrome deletion in p53 mutant mice enhances apoptotic and anti-tumorigenic responses to UV damage at the transcriptome level.Functional & integrative genomics · 2019Article
- Mutation of the gene encoding the circadian clock component PERIOD2 in oncogenic cells confers chemoresistance by up-regulating theThe Journal of biological chemistry · 2019Article
- Opposite Carcinogenic Effects of Circadian Clock Gene BMAL1.Scientific reports · 2018Article
- REV-ERBα reduction is associated with clinicopathological features and prognosis in human gastric cancer.Oncology letters · 2018Article
- Aberrant rhythmic expression ofOncotarget · 2017Article
- Systems Chronotherapeutics.Pharmacological reviews · 2017Review
- Animal Cryptochromes: Divergent Roles in Light Perception, Circadian Timekeeping and Beyond.Photochemistry and photobiology · 2017Review
- Impact of the Circadian Clock on UV-Induced DNA Damage Response and Photocarcinogenesis.Photochemistry and photobiology · 2017Review
- CRY2 and FBXL3 Cooperatively Degrade c-MYC.Molecular cell · 2016Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
The circadian clock in mammalian organisms is generated by a transcription-translation feedback loop that controls many biochemical pathways at the cellular level and physiology and behavior at the organismal level. Cryptochrome (Cry) is a key protein in the negative arm of the transcription-translation feedback loop. It has been found that Cry mutation in cells with p53-null genotype increased their sensitivity to apoptosis by genotoxic agents. Here we show that this increased sensitivity is due to up-regulation of the p53 gene family member p73 in response to DNA damage. As a consequence, when tumors arising from oncogenic Ras-transformed p53(-/-) and p53(-/-)Cry1(-/-)Cry2(-/-) cells are treated with the anticancer drug oxaliplatin, p53(-/-) tumors continue to grow whereas p53(-/-)Cry1(-/-)Cry2(-/-) tumors exhibit extensive apoptosis and stop growing. This finding provides a mechanistic foundation for overcoming the resistance of p53-deficient tumor cells to apoptosis induced by DNA-damaging agents and suggests that disruption of cryptochrome function may increase the sensitivity of tumors with p53 mutation to chemotherapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.