ArticleOncotarget2016
Activation of anaphase-promoting complex by p53 induces a state of dormancy in cancer cells against chemotherapeutic stress.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Cancer Cell Dormancy and Chemotherapy Resistance.Journal of Cancer · 2026Review
- Review
- Advances in the molecular regulation mechanism of tumor dormancy and its therapeutic strategy.Discover oncology · 2024Review
- Dormant cancer cells and polyploid giant cancer cells: The roots of cancer recurrence and metastasis.Clinical and translational medicine · 2024Review
- Targeting the anaphase-promoting complex/cyclosome (APC/C) enhanced antiproliferative and apoptotic response in bladder cancer.Saudi journal of biological sciences · 2023Article
- Immunohistochemical Expression Analysis of Caldesmon Isoforms in Colorectal Carcinoma Reveals Interesting Correlations with Tumor Characteristics.International journal of molecular sciences · 2023Article
- Review
- Emerging role of caldesmon in cancer: A potential biomarker for colorectal cancer and other cancers.World journal of gastrointestinal oncology · 2022Review
- p53 wild-type colorectal cancer cells that express a fetal gene signature are associated with metastasis and poor prognosis.Nature communications · 2022Article
- Detection of Cellular Senescence in Human Primary Melanocytes and Malignant Melanoma Cells In Vitro.Cells · 2022Article
- Cannabidiol Induces Cell Death in Human Lung Cancer Cells and Cancer Stem Cells.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Identifying of biomarkers associated with gastric cancer based on 11 topological analysis methods of CytoHubba.Scientific reports · 2021Article
- Autophagy and Cancer Dormancy.Frontiers in oncology · 2021Review
- Regulation of Formation, Stemness and Therapeutic Resistance of Cancer Stem Cells.Frontiers in cell and developmental biology · 2021Review
- Impact of the Tumor Microenvironment on Tumor Heterogeneity and Consequences for Cancer Cell Plasticity and Stemness.Cancers · 2020Review
- Epithelial-Mesenchymal Transition Programs and Cancer Stem Cell Phenotypes: Mediators of Breast Cancer Therapy Resistance.Molecular cancer research : MCR · 2020Review
- Prevention of cancer dormancy by Fbxw7 ablation eradicates disseminated tumor cells.JCI insight · 2019Article
- The IncRNA BORG: A novel inducer of TNBC metastasis, chemoresistance, and disease recurrence.Journal of cancer metastasis and treatment · 2019Article
- Silencing ofFrontiers in cell and developmental biology · 2019Article
- miR-18a reactivates the Epstein-Barr virus through defective DNA damage response and promotes genomic instability in EBV-associated lymphomas.BMC cancer · 2018Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer dormancy is a stage in tumor progression in which residual disease remains occult and asymptomatic for a prolonged period. Cancer cell dormancy is the main cause of cancer recurrence and failure of therapy. However, cancer dormancy is poorly characterized and the mechanisms of how cancer cells develop dormancy and relapse remain elusive. In this study, 5- fluorouracil (5-FU) was used to induce cancer cell dormancy. We found that cancer cells escape the cytotoxicity of 5-FU by becoming "dormant". After exposure to 5-FU, residual non-small cell lung cancer (NSCLC) cells underwent epithelial-mesenchymal transition (EMT), followed by mesenchymal-epithelial transition (MET). These EMT-transformed NSCLC cells were in the state of cell quiescence where cells were not dividing and were arrested in the cell cycle in G0-G1. The dormant cells underwent an EMT showed characteristics of cancer stem cells. P53 is strongly accumulated in response to 5-FU-induced dormant cells through the activation of ubiquitin ligase anaphase-promoting complex (APC/C) and TGF-β/Smad signaling. In contrast to the EMT-transformed cells, MET-transformed cells showed an increased ability to proliferate, suggesting that dormant EMT cells were reactivated in the MET process. During the EMT-MET process, DNA repair including nonhomologous end joining (NHEJ) and homologous recombination (HR) is critical to dormant cell reactivation. Our findings provide a mechanism to unravel cancer cell dormancy and reactivation of the cancer cell population.
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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.