ArticleBritish journal of cancer2013
Oxidative stress specifically downregulates survivin to promote breast tumour formation.
Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed, 35 citations in OpenAlex.
- Reactive Oxygen Species in Breast Cancer: From Redox Dysregulation to ROS-Responsive Therapeutics.Cell biochemistry and function · 2026Review
- Pharmacological Insights intoMolecules (Basel, Switzerland) · 2026Review
- Cicer arietinum extract as antitumor and protective agent against Ehrlich Solid Carcinoma-bearing mice.BMC complementary medicine and therapies · 2025Article
- Gene Expression and Prognostic Value of NADPH Oxidase Enzymes in Breast Cancer.International journal of molecular sciences · 2024Article
- NADPH Oxidases: From Molecular Mechanisms to Current Inhibitors.Journal of medicinal chemistry · 2023Review
- A Stochastic Binary Model for the Regulation of Gene Expression to Investigate Responses to Gene Therapy.Cancers · 2022Article
- Generation of reactive oxygen species is the primary mode of action and cause of survivin suppression by sepantronium bromide (YM155).RSC medicinal chemistry · 2021Article
- Inhibition of survivin induces spindle disorganization, chromosome misalignment, and DNA damage during mouse embryo development.Cell cycle (Georgetown, Tex.) · 2020Article
- Inhibition of NADPH oxidase alleviates germ cell apoptosis and ER stress during testicular ischemia reperfusion injury.Saudi journal of biological sciences · 2020Article
- Targeting the MAPK/ERK and PI3K/AKT Signaling Pathways Affects NRF2, Trx and GSH Antioxidant Systems in Leukemia Cells.Antioxidants (Basel, Switzerland) · 2020Article
- DUSP9-mediated reduction of pERK1/2 supports cancer stem cell-like traits and promotes triple negative breast cancer.American journal of cancer research · 2020Article
- Nicotine Synergizes with High-Fat Diet to Induce an Anti-Inflammatory Microenvironment to Promote Breast Tumor Growth.Mediators of inflammation · 2020Article
- Modulation of Respiration and Mitochondrial Dynamics by SMAC-Mimetics for Combination Therapy in Chemoresistant Cancer.Theranostics · 2019Article
- Potential Involvement ofOxidative medicine and cellular longevity · 2019Article
- TP53 Mutational Status and ROS Effect the Expression of the Survivin-Associated Radio-Adaptive Response.Radiation research · 2017Article
- Spectrum of spontaneous photon emission as a promising biophysical indicator for breast cancer research.Scientific reports · 2017Article
- Altered expression of a metformin-mediated radiation response in SA-NH and FSa tumor cells treated under in vitro and in vivo growth conditions.International journal of radiation biology · 2017Article
- Very low doses of ionizing radiation and redox associated modifiers affect survivin-associated changes in radiation sensitivity.Free radical biology & medicine · 2016Article
- Pro-Apoptotic Activity of New Honokiol/Triphenylmethane Analogues in B-Cell Lymphoid Malignancies.Molecules (Basel, Switzerland) · 2016Article
- Increased sensitivity of African American triple negative breast cancer cells to nitric oxide-induced mitochondria-mediated apoptosis.BMC cancer · 2016Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundBreast cancer, a heterogeneous disease has been broadly classified into oestrogen receptor positive (ER+) or oestrogen receptor negative (ER-) tumour types. Each of these tumours is dependent on specific signalling pathways for their progression. While high levels of survivin, an anti-apoptotic protein, increases aggressive behaviour in ER- breast tumours, oxidative stress (OS) promotes the progression of ER+ breast tumours. Mechanisms and molecular targets by which OS promotes tumourigenesis remain poorly understood.
resultsDETA-NONOate, a nitric oxide (NO)-donor induces OS in breast cancer cell lines by early re-localisation and downregulation of cellular survivin. Using in vivo models of HMLE(HRAS) xenografts and E2-induced breast tumours in ACI rats, we demonstrate that high OS downregulates survivin during initiation of tumourigenesis. Overexpression of survivin in HMLE(HRAS) cells led to a significant delay in tumour initiation and tumour volume in nude mice. This inverse relationship between survivin and OS was also observed in ER+ human breast tumours. We also demonstrate an upregulation of NADPH oxidase-1 (NOX1) and its activating protein p67, which are novel markers of OS in E2-induced tumours in ACI rats and as well as in ER+ human breast tumours.
conclusionOur data, therefore, suggest that downregulation of survivin could be an important early event by which OS initiates breast tumour formation.
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