ArticleToxicology research2016
Valproic acid causes radiosensitivity of breast cancer cells
Article in Toxicology research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 23 citations in OpenAlex.
- VPA mediates bidirectional regulation of cell cycle progression through the PPP2R2A-Chk1 signaling axis in response to HU.Cell death & disease · 2023Article
- Screen identifies fasudil as a radioprotector on human fibroblasts.Toxicology research · 2022Article
- Hormonal and Genetic Regulatory Events in Breast Cancer and Its Therapeutics: Importance of the Steroidogenic Acute Regulatory Protein.Biomedicines · 2022Review
- Valproic Acid Regulates HR and Cell Cycle Through MUS81-pRPA2 Pathway in Response to Hydroxyurea.Frontiers in oncology · 2021Article
- The Valproate Mediates Radio-Bidirectional Regulation Through RFWD3-Dependent Ubiquitination on Rad51.Frontiers in oncology · 2021Article
- Ex vivo radiosensitivity is increased in non-cancer patients taking valproate.BMC neurology · 2020Article
- The prognosis comparison of different molecular subtypes of breast tumors after radiotherapy and the intrinsic reasons for their distinct radiosensitivity.Cancer management and research · 2019Review
- The Effect of VPA on Increasing Radiosensitivity in Osteosarcoma Cells and Primary-Culture Cells from Chemical Carcinogen-Induced Breast Cancer in Rats.International journal of molecular sciences · 2017Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Valproic acid (VPA) is one of the representative compounds of histone deacetylase inhibitors (HDACis) and is used widely for the clinical treatment of epilepsy and other convulsive diseases. Current reports indicate that HDACis may also be an attractive radiosensitizer for some tumor cells; however, it is unknown whether the safe blood concentration of VPA (0.3-0.8 mM) used for the treatment of epilepsy can also induce radiosensitivity in breast cancer cells. In addition, the mechanism by which VPA may induce radiosensitivity in breast cancer cells is yet to be determined. Our results clearly indicated that VPA at a safe dose (0.5 mM) could significantly increase the radiosensitivity of MCF7 breast cancer cells and result in more accumulation of DNA double strand breaks in response to DNA damage. After VPA treatment, the frequencies of homologous recombination (HR) and non-homologous end joining (NHEJ) tested by recombination substrates, pDR-GFP and EJ5-GFP, were dramatically decreased in the cells without the change of the cell cycle profile. It was further found that VPA could inhibit the recruitment of key repair proteins to DNA break areas, such as Rad51, BRCA1, and Ku80. Thus, our results demonstrated that a safe dose of VPA causes radiosensitivity in breast cancer cells through disrupting the molecular mechanisms of both BRCA1-Rad51-mediated HR and Ku80-mediated NHEJ pathways.
Identifiers
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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.