ArticleCell cycle (Georgetown, Tex.)2013
Ras-induced ROS upregulation affecting cell proliferation is connected with cell type-specific alterations of HSF1/SESN3/p21Cip1/WAF1 pathways.
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 33 papers.
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33 citing papers in PubMed, 54 citations in OpenAlex.
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- Potential Protective Effect of Carotid Endarterectomy: Inducing Ischemic Tolerance in Brain Tissue after Stroke.Journal of molecular neuroscience : MN · 2026Article
- A recombinant humanized type III collagen coating with anti-inflammatory and endothelialization-promoting effects for left atrial appendage closure devices.Regenerative biomaterials · 2026Article
- NPRL2 is required for proliferation of oncogenic Ras-transformed bronchial epithelial cells.Cell division · 2024Article
- Whole-exome sequencing identified recurrent and novel variants in benzene-induced leukemia.BMC medical genomics · 2023Article
- Morphological and Molecular Responses ofInternational journal of molecular sciences · 2022Article
- Article
- Reactive Oxygen Species Bridge the Gap between Chronic Inflammation and Tumor Development.Oxidative medicine and cellular longevity · 2022Review
- An effective method to generate controllable levels of ROS for the enhancement of HUVEC proliferation using a chlorin e6-immobilized PET film as a photo-functional biomaterial.Regenerative biomaterials · 2021Article
- Lipid Metabolism Regulates Oxidative Stress and Ferroptosis in RAS-Driven Cancers: A Perspective on Cancer Progression and Therapy.Frontiers in molecular biosciences · 2021Review
- The Promoting Effect of Traumatic Brain Injury on the Incidence and Progression of Glioma: A Review of Clinical and Experimental Research.Journal of inflammation research · 2021Review
- Oleanolic acid ameliorates intestinal alterations associated with EAE.Journal of neuroinflammation · 2020Article
- Review
- Ferroptosis: Final destination for cancer?Cell proliferation · 2020Review
- Heat shock proteins in the physiology and pathophysiology of epidermal keratinocytes.Cell stress & chaperones · 2019Review
- Cysteine-based regulation of redox-sensitive Ras small GTPases.Redox biology · 2019Review
- Investigating the Effects of Stove Emissions on Ocular and Cancer Cells.Scientific reports · 2019Article
- MiR-16-5p targets SESN1 to regulate the p53 signaling pathway, affecting myoblast proliferation and apoptosis, and is involved in myoblast differentiation.Cell death & disease · 2018Article
- Increased Reactive Oxygen Species and Cell Cycle Defects Contribute to Anemia in the RASA3 Mutant Mouse Model sFrontiers in physiology · 2018Article
- KRas, ROS and the initiation of pancreatic cancer.Small GTPases · 2017Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncogenes of the RAS family regulate many of the cell's activities, including proliferation, survival and differentiation. Activating mutations in these genes are common events for many types of cancer. One of the contradictory points concerning the biological significance of Ras activation is its dual effect (pro- or anti-proliferative) on cell reproduction. One of mechanisms by which Ras proteins influence cell growth is a regulation of intracellular level of reactive oxygen species (ROS), second messengers affecting variety of cellular processes including cell proliferation. Recently it was shown that repression of SESN1 and SESN3 genes, whose protein products control regeneration of peroxiredoxins, can play a critical role in Ras-induced ROS upregulation. In the present study we have found that Ras-induced repression of SESN3 expression and ROS upregulation is mediated via the modifications of transcriptional activity of HSF1. Interestingly, mutant Ras overexpression altered the activity of HSF1 in opposite directions in different cell contexts, in particular in human normal fibroblasts and HaCaT immortalized keratinocytes, but these opposite changes caused similar repression of SESN3 expression followed by elevation of ROS content and inhibition of cell proliferation in corresponding cell types. The inhibitory effect on cell proliferation was mediated by upregulation of p21(Cip1/WAF1). Thus, HSF1/SESN3/ROS/p21(Cip1/WAF1)-mediated deceleration of cell growth may contribute to cell defense systems protecting the organism from excessive proliferation of cells that overexpress activated Ras oncoproteins.
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