ArticleJournal of inflammation (London, England)2015
Inflammation contributes to NKX3.1 loss and augments DNA damage but does not alter the DNA damage response via increased SIRT1 expression.
Article in Journal of inflammation (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Molecular Sentinels: Unveiling the Role of Sirtuins in Prostate Cancer Progression.International journal of molecular sciences · 2024Review
- Association of interleukin-17A and chemokine/vascular endothelial growth factor-induced angiogenesis in newly diagnosed patients with bladder cancer.BMC immunology · 2024Article
- Dehydrozingerone promotes healing of diabetic foot ulcers: a molecular insight.Journal of cell communication and signaling · 2023Article
- Androgen receptor contributes to repairing DNA damage induced by inflammation and oxidative stress in prostate cancer.Turkish journal of biology = Turk biyoloji dergisi · 2023Article
- Applications of Vertebrate Models in Studying Prostatitis and Inflammation-Associated Prostatic Diseases.Frontiers in molecular biosciences · 2022Review
- Berberine Encapsulated Lecithin-Chitosan Nanoparticles as Innovative Wound Healing Agent in Type II Diabetes.Pharmaceutics · 2021Article
- Nutlin3a-Loaded Nanoparticles Show Enhanced Apoptotic Activity on Prostate Cancer Cells.Molecular biotechnology · 2019Article
- Article
- GPX3 suppresses tumor migration and invasion via the FAK/AKT pathway in esophageal squamous cell carcinoma.American journal of translational research · 2018Article
- Sinomenine Induces G1-Phase Cell Cycle Arrest and Apoptosis in Malignant Glioma Cells Via Downregulation of Sirtuin 1 and Induction of p53 Acetylation.Technology in cancer research & treatment · 2018Article
- Oxidative stress and prostatic diseases.Molecular and clinical oncology · 2017Article
- European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS).Redox biology · 2017Review
- Th17 Cells in Protection from Tumor or Promotion of Tumor Progression.Journal of clinical & cellular immunology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The oxidative stress response is a cellular defense mechanism that protects cells from oxidative damage and cancer development. The exact molecular mechanism by which reactive oxygen species (ROS) contribute to DNA damage and increase genome instability in prostate cancer merits further investigation. Here, we aimed to determine the effects of NKX3.1 loss on antioxidant defense in response to acute and chronic inflammation in an in vitro model. Oxidative stress-induced DNA damage resulted in increased H2AX((S139)) phosphorylation (a hallmark of DNA damage), along with the degradation of the androgen receptor (AR), p53 and NKX3.1, upon treatment with conditioned medium (CM) obtained from activated macrophages or H2O2. Furthermore, the expression and stability of SIRT1 were increased by CM treatment but not by H2O2 treatment, although the level of ATM((S1981)) phosphorylation was not changed compared with controls. Moreover, the deregulated antioxidant response resulted in upregulation of the pro-oxidant QSCN6 and the antioxidant GPX2 and downregulation of the antioxidant GPX3 after CM treatment. Consistently, the intracellular ROS level increased after chronic treatment, leading to a dose-dependent increase in the ability of LNCaP cells to tolerate oxidative damage. These data suggest that the inflammatory microenvironment is a major factor contributing to DNA damage and the deregulation of the oxidative stress response, which may be the underlying cause of the increased genetic heterogeneity during prostate tumor progression.
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