ReviewTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Estrogen potentiates reactive oxygen species (ROS) tolerance to initiate carcinogenesis and promote cancer malignant transformation.
Review in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it.
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- Anemia and Its Connections to Inflammation in Older Adults: A Review.Journal of clinical medicine · 2024Review
- G protein-coupled estrogen receptor activates PI3K/AKT/mTOR signaling to suppress ferroptosis via SREBP1/SCD1-mediated lipogenesis.Molecular medicine (Cambridge, Mass.) · 2024Article
- Association between composite dietary antioxidant index and migraine in American young women: insights from NHANES 1999-2004 cross-sectional data.Frontiers in neurology · 2024Article
- AQP3 Promotes the Invasion and Metastasis in Cervical Cancer by Regulating NOX4-derived HJournal of Cancer · 2024Article
- Ferroptosis, Metabolic Rewiring, and Endometrial Cancer.International journal of molecular sciences · 2023Review
- A View on Uterine Leiomyoma Genesis through the Prism of Genetic, Epigenetic and Cellular Heterogeneity.International journal of molecular sciences · 2023Review
- Antioxidative, Anti-Inflammatory, Anti-Obesogenic, and Antidiabetic Properties of Tea Polyphenols-The Positive Impact of Regular Tea Consumption as an Element of Prophylaxis and Pharmacotherapy Support in Endometrial Cancer.International journal of molecular sciences · 2022Review
- The power of heteronemin in cancers.Journal of biomedical science · 2022Review
- Promoter hypomethylation and overexpression of TSTD1 mediate poor treatment response in breast cancer.Frontiers in oncology · 2022Article
- Effect of Estrogen on Heteronemin-Induced Anti-proliferative Effect in Breast Cancer Cells With Different Estrogen Receptor Status.Frontiers in cell and developmental biology · 2021Article
- Prognostic Model for Predicting Overall and Cancer-Specific Survival Among Patients With Cervical Squamous Cell Carcinoma: A SEER Based Study.Frontiers in oncology · 2021Article
- Matrix Softness-Mediated 3D Zebrafish Hepatocyte Modulates Response to Endocrine Disrupting Chemicals.Environmental science & technology · 2020Article
- MicroRNA and Oxidative Stress Interplay in the Context of Breast Cancer Pathogenesis.International journal of molecular sciences · 2019Review
- Effect of radiotherapy on the survival of cervical cancer patients: An analysis based on SEER database.Medicine · 2019Article
- Sulforaphane-induced metabolomic responses with epigenetic changes in estrogen receptor positive breast cancer cells.FEBS open bio · 2018Article
- Ethyl β-Carboline-3-Carboxylate Increases Cervical Cancer Cell Apoptosis Through ROS-p38 MAPK Signaling Pathway.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Estrogen-mediated high reactive oxygen species (ROS) tolerance plays an important role in driving carcinogenesis. ROS overproduction acts as the significant effector to increase genomic instability and transduce redox-related signal pathway. Especially, estrogen-mediated mitochondrial ROS promote the mutations in mitochondrial DNA (mtDNA) and the damage to mitochondrial proteins. Moreover, estrogen-mediated ROS contribute to the alteration of energy metabolism and modulate several redox-sensitive proteins responsible for cell proliferation and anti-apoptosis. On the other hand, estrogen simultaneously performs the antioxidative beneficial functions, which protects cancer cells from the potential cytotoxic effects of estrogen-mediated ROS through activation of nuclear factor-erythroid-2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1) antioxidant response. Consequently, estrogen potentiates the high ROS tolerance through increase of ROS production as well as acceleration of ROS elimination, which ultimately results in estrogen-mediated carcinogenesis and malignant transformation. However, this overdependence on antioxidant response system to resist ROS-mediated cytotoxicity also represents the "Achilles' Heel" of estrogen-mediated cancer cells. In other words, the destruction of the high ROS tolerance using antioxidant inhibitors may provide a novel and efficacious measure to selectively eliminate these cancer cells without harming normal cells. Of course, it will be necessary to define the exact situation of ROS homeostasis in the different cellular microenvironment and further decipher the mechanisms of redox regulation, which is consequently used as a new avenue to optimize the clinical therapy for estrogen-mediated cancer.
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