ArticleCell cycle (Georgetown, Tex.)2013
Cyclin D1 overexpression perturbs DNA replication and induces replication-associated DNA double-strand breaks in acquired radioresistant cells.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 79 citations in OpenAlex.
- Inhibiting cyclin D1-CDK6 suppresses senescence-associated inflammatory gene expression and age-related functional decline.Nature aging · 2026Article
- Synthesis, characterization of Mg doped CuFeScientific reports · 2026Article
- Cyclin D1 expression predicts mismatch repair deficiency and correlates significantly with overall survival and recurrence free survival in endometrial carcinoma.Journal of molecular histology · 2025Article
- Cyclin D1 overexpression induces replication stress and microhomology-mediated end-joining dependence in mantle cell lymphoma.The Journal of clinical investigation · 2025Article
- Article
- The PRC2.1 Subcomplex Opposes G1 Progression through Regulation of CCND1 and CCND2.bioRxiv : the preprint server for biology · 2024Article
- The prostaglandin EAmerican journal of physiology. Endocrinology and metabolism · 2024Article
- D-Type Cyclins in Development and Disease.Genes · 2023Review
- Article
- Degradation strategy of cyclin D1 in cancer cells and the potential clinical application.Frontiers in oncology · 2022Review
- The Oncogenic and Diagnostic Potential of Stanniocalcin 2 in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2022Article
- Cancer-associated fibroblasts promote the survival of irradiated nasopharyngeal carcinoma cells via the NF-κB pathway.Journal of experimental & clinical cancer research : CR · 2021Article
- Mechanism of turnover or persistence of radiation-induced myofibroblast in vitro.Cell cycle (Georgetown, Tex.) · 2020Article
- Eliminating Radiation Resistance of Non-Small Cell Lung Cancer by Dihydroartemisinin Through Abrogating Immunity Escaping and Promoting Radiation Sensitivity by Inhibiting PD-L1 Expression.Frontiers in oncology · 2020Article
- The double dealing of cyclin D1.Cell cycle (Georgetown, Tex.) · 2020Review
- Review
- Mistletoe-Based Drugs Work in Synergy with Radio-Chemotherapy in the Treatment of GliomaEvidence-based complementary and alternative medicine : eCAM · 2019Article
- Difference in Acquired Radioresistance Induction Between Repeated Photon and Particle Irradiation.Frontiers in oncology · 2019Review
- Hint1 expression inhibits proliferation and promotes radiosensitivity of human SGC7901 gastric cancer cells.Oncology letters · 2018Article
- Clinically relevant radioresistant cell line: a simple model to understand cancer radioresistance.Medical molecular morphology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fractionated radiotherapy (RT) is widely used in cancer treatment, because it preserves normal tissues. However, repopulation of radioresistant tumors during fractionated RT limits the efficacy of RT. We recently demonstrated that a moderate level of long-term fractionated radiation confers acquired radioresistance to tumor cells, which is caused by DNA-PK/AKT/GSK3β-mediated cyclin D1 overexpression. The resulting cyclin D1 overexpression leads to forced progression of the cell cycle to S-phase, concomitant with induction of DNA double-strand breaks (DSBs). In this study, we investigated the molecular mechanisms underlying cyclin D1 overexpression-induced DSBs during DNA replication in acquired radioresistant cells. DNA fiber data demonstrated that replication forks progressed slowly in acquired radioresistant cells compared with corresponding parental cells in HepG2 and HeLa cell lines. Slowly progressing replication forks were also observed in HepG2 and HeLa cells that overexpressed a nondegradable cyclin D1 mutant. We also found that knockdown of Mus81 endonuclease, which is responsible for resolving aberrant replication forks, suppressed DSB formation in acquired radioresistant cells. Consequently, Mus81 created DSBs to remove aberrant replication forks in response to replication perturbation triggered by cyclin D1 overexpression. After treating cells with a specific inhibitor for DNA-PK or ATM, apoptosis rates increased in acquired radioresistant cells but not in parental cells by inhibiting the DNA damage response to cyclin D1-mediated DSBs. This suggested that these inhibitors might eradicate acquired radioresistant cells and improve fractionated RT outcomes.
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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.