Blood 105(11):41634169, Haraguchi N et al (2010) CD13 is a therapeutic target in human liver cancer stem cells. A novel platinum complex containing a piplartine derivative exhibits enhanced cytotoxicity, causes oxidative stress and triggers apoptotic cell death by ERK/p38 pathway in human acute promyelocytic leukemia HL-60 cells. Gopalakrishna, R. & Jaken, S. Protein kinase C signaling and oxidative stress. Drugs 24, 7994 (2015). For example, ROS, via oxidation of thioredoxin, enhance the nuclear localization of both the ataxia-telangiectasia mutated (ATM) serine/threonine kinase, which is involved in DNA damage repair31,32, and redox factor-1 (Ref-1), a multifunctional protein that enables Fos/Jun DNA-binding and is identical to the apurinic/apyrimidinic 1 (APE1) endonuclease33. Nat. Therefore, the role of p53 in this context appears to be different from that reported in several studies showing that it decreases the levels of ROS. Cell Metab 28(1):6986.e66, Lupia M, Cavallaro U (2017) Ovarian cancer stem cells: still an elusive entity? Commun. These pathways mediated by ROS have been targeted by various blockers, stimulators, and inhibitors, and in many cases, promising results have been found. Toxicol Appl Pharmacol 364:1221, Duan D et al (2014) Shikonin targets cytosolic thioredoxin reductase to induce ROS-mediated apoptosis in human promyelocytic leukemia HL-60 cells. Finally, the most recent ROS-inducing drugs have addressed the pivotal goal of therapists: cancer selectivity. Biochem Pharmacol 148:6474, Wu S et al (2019) Nrf2 in cancers: a double-edged sword. The production of reactive oxygen species (ROS) was measured by fluorescence microscopy and flow cytometry. Proc Natl Acad Sci 105(19):69246929, Wu T et al (2015) Oxidative stress, mammospheres and Nrf2new implication for breast cancer therapy? ROS production was also increased in the presence of some anticancer drugs, such as vinblastine, but not by others. 7, 11111117 (2001). Cell Stem Cell 12(3):329341, Lapidot T et al (1994) A cell initiating human acute myeloid leukaemia after transplantation into SCID mice. 42, 804821 (2014). Mol. Cancer Res 70(6):25162527, Junttila MR, de Sauvage FJ (2013) Influence of tumour micro-environment heterogeneity on therapeutic response. Cell 178, 330345 (2019). BACH1 stabilization by antioxidants stimulates lung cancer metastasis. Sci. official website and that any information you provide is encrypted Carousel with three slides shown at a time. Bethesda, MD 20894, Web Policies Oncogene 32(40):48254835, CrossRef ROS also influence the activity of calcium channels; in fact, they induce the release of calcium from cellular stores with the consequent activation of kinases, such as protein kinase C (PKC), thereby playing important roles in the proliferation of cancer cells18. 7, 18751884 (2008). Science 275, 16491652 (1997). Circ. Curr. Mol. Cytochrome c acts as a cardiolipin oxygenase required for release of proapoptotic factors. Keywords: Cancer Cell 23(3):316331, Dong J et al (2019) Cordycepin sensitizes breast cancer cells toward irradiation through elevating ROS production involving Nrf2. Oncogene-induced Nrf2 transcription promotes ROS detoxification and tumorigenesis. Oncogene 32(22):27672781, Chen K et al (2013) Acetylation of the cell-fate factor dachshund determines p53 binding and signaling modules in breast cancer. Blood J Am Soc Hematol 113(23):57655775, CAS Cell Res. Biol. 2, 211230 (2010). Clarifying the Real Bioactive Constituents of Garlic1 Harunobu Amagase2,3 Department of Research and Development, Wakunaga of America Co., Mission Viejo, CA 92691. Google Scholar, Baba T et al (2009) Epigenetic regulation of CD133 and tumorigenicity of CD133+ ovarian cancer cells. This may take some time to load. J. Transl. ROS, previously considered mere byproducts of cellular respiration, are oxygen-containing molecules with high reactivity. Wilkie-Grantham, R. P., Matsuzawa, S. & Reed, J. C. Novel phosphorylation and ubiquitination sites regulate reactive oxygen species-dependent degradation of anti-apoptotic c-FLIP protein. A moderate amount of reactive oxygen species (ROS) is produced under normal conditions, where they play an important role in cell signaling and are involved in many aspects of the immune response to pathogens. Reactive oxygen species promote TNF alpha-induced death and sustained JNK activation by inhibiting MAP kinase phosphatases. Cancer, when mostly untreatable, is hypothesizedto be sustained due to the presence of highly self-propagating, therapy-resistant cancer stem cells. If, for any reason, ROS production increases or the number of scavenged ROS decreases, then cells experience a condition known as oxidative stress. Stem Cells Dev 24(4):405416, Myant KB et al (2013) ROS production and NF-B activation triggered by RAC1 facilitate WNT-driven intestinal stem cell proliferation and colorectal cancer initiation. In this regard, to prevent excessive intracellular ROS, cancer cells respond to oxidative stress by inducing the transcription of antioxidant enzymes, highlighting the relevance of an in-depth knowledge of these pathways for use in elaborating therapies that alter ROS levels. Many drugs used in anticancer therapy induce oxidative stress. https://doi.org/10.1038/s41467-018-02915-8 (2018). However, ROS are able to induce DNA hypermethylation as well, with potential consequences on tumor phenotype when promoter regions of tumor suppressor genes are involved43,44,45. Cancer Sci. Cancer Discov. De Raedt, T. et al. Hepatology 58(2):629641, Xu B et al (2017) Disulfiram/copper selectively eradicates AML leukemia stem cells in vitro and in vivo by simultaneous induction of ROS-JNK and inhibition of NF- B and Nrf2. Joyce, J. Proc. Involvement of reactive oxygen species in 2-methoxyestradiol-induced apoptosis in human neuroblastoma cells. Chem. Cancer 2022, 22 (5): 280-297 Eukaryotic cells have developed complex systems to regulate the production and response to reactive oxygen species (ROS). NOV-002, a glutathione disulfide mimetic, as a modulator of cellular redox balance. Toxicol Appl Pharmacol 244(1):6676, Lagadinou ED et al (2013) BCL-2 inhibition targets oxidative phosphorylation and selectively eradicates quiescent human leukemia stem cells. Oncoimmunology 5, e1080416 (2015). Cancer Sci 107(7):9911000, Thomas S et al (2012) CD24 is an effector of HIF-1driven primary tumor growth and metastasis. ROS generated after the formation of ceramide or after an increase in energy metabolism induced by several receptor-interacting protein kinases (RIPs), either in the mitochondrial ETC and/or by NOXs, have been reported to enhance necroptosis123,124,125. Cancer 9, 239252 (2009). Proc. Diehn, M. et al. DNA damage and repair modify DNA methylation and chromatin domain of the targeted locus: mechanism of allele methylation polymorphism. 5, 219234 (2006). This study was supported by Italian Ministry of University and Scientific Research [P.R.I.N. Free Rad. https://doi.org/10.14348/molcells.2016.2327 (2016). Together, these modifications, induced by coordinated targeting of transcription factors that is currently referred to as epigenetic marks, conform to a precise code with specific time requirements to control whole gene expression139. & Leonard, W. J. Modulation of transcription factor NF-kappa B binding activity by oxidation-reduction in vitro. Their proportion within the tumor is not known, nor any exact correlation could be drawn between the proportion of cancer stem cells in a tumor and the aggressiveness of the metastatic disease. ROS are also continuously generated by enzymatic reactions involving cyclooxygenases, NADPH oxidases (NOXs), xanthine oxidases and lipoxygenases and through the iron-catalyzed Fenton reaction; indeed, it should be noted that NOXs have primarily evolved to produce ROS2. UVA and UVBinduced production in ROS and reactive nitrogen species contributes to inflammation, immunosuppression, . Cancer Res. Kim, J., Kim, J. Charruyer, A. et al. Med. Article Guo, Z., Kozlov, S., Lavin, M. F., Person, M. D. & Paull, T. T. ATM activation by oxidative stress. Orino, K. et al. sharing sensitive information, make sure youre on a federal & Fanburg, B. L. Activation of an H2O2-generating NADH oxidase in human lung fibroblasts by transforming growth factor beta 1. 36, 3038 (2011). Mol Carcinog 54(11):14941502, Wu Q et al (2018) Ginsenoside Rh4 induces apoptosis and autophagic cell death through activation of the ROS/JNK/p53 pathway in colorectal cancer cells. Science 330, 517521 (2010). Mechanisms of action of arsenic trioxide. Although ROS production is elevated in cancer cells it can also promote a natural process called programmed cell death. Circulation Res. Cancer Res. Shen, B., He, P. J. Print 2023 Feb. Yang Z, Wang X, Hong W, Zhang S, Yang Y, Xia Y, Yang R. Front Pharmacol. CAS Melatonin induces ROS production in cancer cells through calmodulin binding. Biol. The extrinsic pathway is mediated by binding of death-inducing ligands such as TNF and Fas ligand that bind to cognate receptors that, in turn, recruit adaptor proteins and pro-caspases, leading to the assembly of the death-inducing signaling complex (DISC) and the activation of effector caspases75. 87, 245313 (2007). Cancer Res 74(14):38903901, Gang EJ et al (2004) In vitro mesengenic potential of human umbilical cord blood-derived mesenchymal stem cells. Acad. Toledano, M. B. Antioxid Redox Signal 16(11):12151228, Shi Q et al (2015) Sevoflurane promotes the expansion of glioma stem cells through activation of hypoxia-inducible factors in vitro. FOXO transcription factor activation by oxidative stress mediated by the small GTPase Ral and JNK. The current study was designed to investigate the functional role of 3-MST's catalytic activity in the murine colon Cancer cell line CT26. The first approach is based on lowering ROS levels to counteract their role in cellular transformation; it is aimed at reducing the number of transformed cells by depriving them of fuel (represented in the upper right side of the figure as a lower proportion of transformed cells with respect to that of normal cells). Sci. Sci. However, a growing body of evidence supports the view that antioxidant activities are essential for tumorigenesis. Scherz-Shouval, R. et al. Rev. Methods for determining the oncogenic condition of cell, uses thereof, and methods for treating cancer Methods for detecting the oncogenic condition of cells, steps where amount of the 6-oxo-cholestan-3,5-diol (OCDO) compound is measured, uses thereof. Exploring oxidative modifications of tyrosine: an update on mechanisms of formation, advances in analysis and biological consequences. Drug Metab. 21, 1503 (2014). Stem Cells 27(12):28752883, Davidson B (2016) CD24 is highly useful in differentiating high-grade serous carcinoma from benign and malignant mesothelial cells. Nanoparticles produced by plant extracts are more stable and biocompatible in comparison with those produced by physical and chemical methods. The stimulated production of reactive oxygen species by phagocytic cells was originally called "the respiratory burst" due to the increased consumption of oxygen by these cells [8]. Specifically, cellular responses to ROS must be imagined as the integration of multiple levels in which, in addition to their nature and relative concentration, their location plays an important role. Microsc Res Tech. 26, 17491760 (2007). Breast Cancer Res Treat 122(3):777785, Kaplan RN et al (2005) VEGFR1-positive haematopoietic bone marrow progenitors initiate the pre-metastatic niche. These reactive molecules contain an oxygen and include H(2;)O(2;) (hydrogen peroxide), NO (nitric oxide), O(2;)(-) (oxide anion), peroxynitrite (ONOO(-)), hydrochlorous acid (HOCl), and hydroxyl radical (OH(-)). BMC Cancer 19(1):618, Deroanne CF et al (1997) Angiogenesis by fibroblast growth factor 4 is mediated through an autocrine up-regulation of vascular endothelial growth factor expression. This is a preview of subscription content, access via your institution. government site. Biol. The results show that intracellular ROS production increases up to 90% following upon the exposure of AMF to HepG2 cells containing BMNPs, which could determine the loss of cell viability (up to 40% reduction) without a significant rise in temperature. This review considers the role of ROS in the various stages of cancer development. Hanahan, D. & Weinberg, R. A. Hallmarks of cancer: the next generation. Anticancer Res 23(5a):39853990, CAS Gupta SC, Hevia D, Patchva S, Park B, Koh W, Aggarwal BB. 53, 615627 (2002). In fact, it has been found that the breast cancer susceptibility 1 (BRCA1) gene interacts with and induces Nrf2 expression with positive outcomes on cancer cell survival63. Grollman, A. P. & Moriya, M. Mutagenesis by 8-oxoguanine: an enemy within. ROS modulate various cell signaling pathways, which are primarily mediated through the transcription factors NF-B and STAT3, hypoxia-inducible factor-1, kinases, growth factors, cytokines and other proteins, and enzymes; these pathways have been linked to cellular transformation, inflammation, tumor survival, proliferation, invasion, angiogenesis, and metastasis of cancer. PubMed ROS Production Determination. Google Scholar. Prieto-Bermejo, R., Romo-Gonzalez, M., Perez-Fernandez, A., Ijurko, C. & Hernandez-Hernandez, A. Reactive oxygen species in hematopoiesis: leukemic cells take a walk on the wild side. CSCs possess enhanced protection capabilities to maintain reduced intracellular levels of reactive oxygen species (ROS) compared with nonstem-like cancer cells. Gastroenterology 141(6):22182227.e2215, Li B et al (2019) Targeting glutaminase 1 attenuates stemness properties in hepatocellular carcinoma by increasing reactive oxygen species and suppressing Wnt/beta-catenin pathway. Custom Antibody Labeling. Cell Death Differ. 38, 15851593 (2005). These pumps belong to the adenosine triphosphate (ATP)-binding cassette (ABC) transporter superfamily and are dependent on intracellular ATP stores135. Finkel, T. Signal transduction by reactive oxygen species. PubMedGoogle Scholar. Tight regulation of ROS levels is crucial for cellular life; in fact, moderate ROS contribute to the control of cell proliferation and differentiation. Furthermore, platinum-based drugs elevate ROS levels that promote PCD; protocols for the administration of these compounds in combination with inhibitors of poly(ADP-ribose) polymerase (PARP), which is involved in the maintenance of DNA integrity, have been shown to arrest the growth of breast cancer cells, even in BRCA-deficient models106,107. In this article we propose several simple, fast, and affordable assays; these assays have been validated by many publications and are routinely used to detect ROS or its effects in mammalian cells. USA 95, 79877992 (1998). 180, 30723080 (2008). Sci. 280, 19441965 (2013). Inside the Cell 1(2):96105, Carpenter PM, Dao AV (2003) The role of hyaluronan in mesothelium-induced motility of ovarian carcinoma cells. official website and that any information you provide is encrypted Data https://doi.org/10.1038/sdata.2017.43 (2017)-. Unrepaired 8-oxo-G is potentially one of the most mutagenic lesions, since it pairs with A, inducing GT transversions40, and represents a prominent candidate to be a marker of ROS-induced mutagenesis and tumorigenesis41. Nat. Nat. 2013 Feb 8;1(1):244-57. doi: 10.1016/j.redox.2013.01.014. Med. Sci. Fetching data from CrossRef. NPJ Precis Oncol 2(1):113, Magenta A et al (2011) miR-200c is upregulated by oxidative stress and induces endothelial cell apoptosis and senescence via ZEB1 inhibition. 2016;81:163-175. doi: 10.1101/sqb.2016.81.030791. Epub 2020 Apr 23. Evid Based Complement Alternat Med 2013:590393, Shi X et al (2012) Reactive oxygen species in cancer stem cells. Annu. Morano, A. et al. PubMed They are produced in many cellular compartments and play a major role in signaling pathways. Essers, M. A. et al. Nat. J Biosci Bioeng 118(2):214222, Chen W et al (2016) Cancer stem cell quiescence and plasticity as major challenges in cancer therapy. Tumori Journal 96(6):985992, Zhang S et al (2012) The roles of hypoxia-inducible factors in regulating neural stem cells migration to glioma stem cells and determinating their fates. Association of reactive oxygen species levels and radioresistance in cancer stem cells. Epub 2017 Jan 12. J Biol Chem 276(52):4867948692, Brandon M et al (2006) Mitochondrial mutations in cancer. Mol. Cancer Res. 6, 221ra215 (2014). https://doi.org/10.1007/978-981-15-9411-3_123, Handbook of Oxidative Stress in Cancer: Mechanistic Aspects, Shipping restrictions may apply, check to see if you are impacted, Reference Module Biomedical and Life Sciences, Tax calculation will be finalised during checkout. Chem. HHS Vulnerability Disclosure, Help ROS are also able to induce necrosis, which was originally considered an unregulated form of cell death but is now recognized as type III programmed cell death (necroptosis)121,122. J. Biol. 2010) In agreements with others . Cancer Cell 19(3):387400, Islam F et al (2019) Cancer stem cells: role in tumor progression and treatment resistance. This process is potentially dangerous to cells, as peroxidation of mitochondrial phospholipids may affect the integrity of permeability transition pores (PTPs) and disaggregate complexes I and III of the respiratory chain, thereby enhancing electron leakage within the mitochondrial intermembrane space5,6. Moreover, increased intracellular levels of GSH are required for the initiation and progression of various types of cancer, and inhibitors of GR behave as anticancer drugs66, while high levels of NADPH boost the metastatic ability of melanoma cells, and protocols based on depletion of GSH (isothiocyanates and aziridine derivatives that bind GSH) or based on blocking the uptake of a rate-limiting precursor of its synthesis (inhibitors of the cysteine/glutamate antiporter, XCT) greatly impact cancer cell survival67,68. Reactive oxygen species (ROS) are by-products of normal cell activity. 8, 836845 (2002). Oxidative stress has been implicated in the pathophysiology of cancer: in fact, high levels of ROS generated by ongoing aerobic glycolysis followed by pyruvate oxidation in mitochondria (the Warburg effect), increase receptor and oncogene activity, and the stimulation of growth factor-dependent pathways or oxidizing enzymes induce genetic instability3,4. 208, 167174 (2018). & Huang, P. Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach? Perillo, B. et al. 2017 Mar;104:144-164. doi: 10.1016/j.freeradbiomed.2017.01.004. Galadari S, Rahman A, Pallichankandy S, Thayyullathil F. Free Radic Biol Med. Decrease in mitochondrial complex I activity in ischemic/reperfused rat heart: involvement of reactive oxygen species and cardiolipin. L.M. eCollection 2022. J. Upon pathogen recognition and engulfment, the NOX complex is formed within the phagosomal membranes, and it converts molecular oxygen into a highly reactive oxygen intermediatesuperoxide [ 2 ]. Article Jadaun P, Seniya C, Pal SK, Kumar S, Kumar P, Nema V, Kulkarni SS, Mukherjee A. Antioxidants (Basel). ROS influence the activity of epigenetic modulators, such as histone deacetylases (HDACs) or DNA methyltransferases (DNMTs) with consequences that are evident in the expression of the target genes38,39. UV-C light induces raft-associated acid sphingomyelinase and JNK activation and translocation independently on a nuclear signal. These functions are intimately linked to mitochondrial morphology, which is highly dynamic and capable of rapid and transient changes to alter cellular functions in response to environmental cues and cellular demands. Proc. They also oxidize DNA, especially adenine and guanine (8-oxo-A and 8-oxo-G). The major signaling cascades induced by growth factor-stimulated ROS are highlighted on the left. The main consequences of oxidative stress in cancer cells are illustrated on the right. Cancer Res. PMC Nature 494, 361365 (2013). Proc Natl Acad Sci 105(33):1166711672, Chang W-W et al (2013) The expression and significance of insulin-like growth factor-1 receptor and its pathway on breast cancer stem/progenitors. Iron-dependent cell death of hepatocellular carcinoma cells exposed to sorafenib. Nucleic Acids Res. In conclusion, the positive correlation of necroptosis with ROS implies that regulating ROS to induce necroptosis in tumor cells is a potential strategy for cancer therapy. Sci. Houee-Levin, C. et al. Cancer Med 8(5):22522267, Xia H et al (2013) MicroRNA-216a/217-induced epithelial-mesenchymal transition targets PTEN and SMAD7 to promote drug resistance and recurrence of liver cancer. Lignitto, L. et al. Moreover, we demonstrated that carnosol significantly induced autophagy and co-administration of autophagy inhibitor reduced the antiproliferating effect of carnosol. Berndtsson, M. et al. Chem. Also, as ROS are an inevitable by-product of metabolism, the increased metabolism sustaining increased proliferation in cancer cells results in increased ROS production. De Nicola, G. M. et al. Oxidative phosphorylation in mitochondria involves four electron-transporting complexes and a proton-translocating ATP synthase that direct electrons derived from the initial oxidation of NADPH and FADH2 along a multistep pathway that culminates in protons being pumped outside of mitochondria. & Gout, P. W. Potential use of the anti-inflammatory drug, sulfasalazine, for targets therapy of pancreatic cancer. Front Cell Dev Biol 5(18), Serakinci N, Keith WN (2006) Therapeutic potential of adult stem cells. Science 270, 296299 (1995). Putker, M. et al. Chem. In addition, a very intriguing ROS-related molecular mechanism of tumor suppression by p53 has recently been highlighted; this protein induces a peculiar form of cell death, now called ferroptosis, via an increase in ROS levels that subsequently inhibit the cystine uptake typically mediated by the repression of a key component of the cystine/glutamate antiporter126. We have previously shown that estrogen-induced transcription is triggered by LSD1-catalyzed demethylation of lysine 9 in histone H3 (H3K9), which is activated by the binding of liganded estrogen receptor to the enhancers of target genes140. Cancer initiation and progression leverage slight increases in ROS levels. Nature 458, 780783 (2009). Scherz-Shouval, R. & Elazar, Z. Cell Biol. PubMed Cancer Prev. The authors discuss molecular mechanisms underlying the potential anti-cancer activity of various ROS-producing strategies, including drugs and light-stimulated therapies. Nanotechnology research is emerging as cutting-edge technology, and nanoparticles (NPs) and nanocomposites (NCs) have played a significant role in the bioremediation and treatment of polluted water by organic and nonorganic materials. Nature 438(7069):820827, Kelly PN et al (2007) Tumor growth need not be driven by rare cancer stem cells. Cancer Res 65(2):465472, Kubben N et al (2016) Repression of the antioxidant NRF2 pathway in premature aging. Biol. PubMed Central The antioxidant paradox. Intuitively, generation of ROS in this process must be timely and spatially controlled to prevent excessive damage to the DNA: a recent report, in fact, describes a new role for the originally discovered superoxide dismutase, SOD1, that is recruited to the nucleus in response to specific stimuli142. Cell Stem Cell 8(1):5971, Lee S-R et al (2002) Reversible inactivation of the tumor suppressor PTEN by H2O2. Med. Part of Springer Nature. You are using a browser version with limited support for CSS. Nature 436, 123127 (2005). 2022 Nov 4;27(1):232. doi: 10.1186/s40001-022-00833-6. CAS You do not have JavaScript enabled. 24, 96959704 (2004). Hodny, Z., Reinis, M., Hubackova, S., Vasicova, P. & Bartek, J. Interferon gamma/NADPH oxidase defense system in immunity and cancer. Life Sci Alliance. Cancer Res 72(1):335345, Bao B et al (2014) Targeting CSCs in tumor microenvironment: the potential role of ROS-associated miRNAs in tumor aggressiveness. Cancer Biol. ROS production was increased with temperature in cancer cells, but not in normal cells; this increase was potently inhibited by ascorbic acid. Google Scholar. Omenn, G. S. et al. Redox Biol. Wang, J. sharing sensitive information, make sure youre on a federal Stem Cells 30(10):23092319, Luo L et al (2011) Ovarian cancer cells with the CD117 phenotype are highly tumorigenic and are related to chemotherapy outcome. 2022 Nov 29;6(2):e202201529. Before Additionally, FOXO transcription factors have recently been implicated in tumorigenesis: in fact, rhabdomyosarcomas present FOXO genes with a high percentage of mutations that render them insensitive to inhibition by AKT signaling65. Ferrodoxin reductase affects p53-dependent, 5-fluorouracil-induced apoptosis in colorectal cancer cells. Nucleic Acids Res. Bookshelf ROS production in phagocytic cells is mainly mediated through the activity of the NOX complex. Role of KEAP1/NRF2 and TP53 mutations in lung squamous cell carcinoma development and radiation resistance. Therapeutic antibodies current state and future trends-is a paradigm change coming soon? It has been reported that ~1 in 105 guanines is oxidized in normal cells and that this proportion is increased by 3550% in transformed cells7. Read more about how to correctly acknowledge RSC content. R01 CA142664/CA/NCI NIH HHS/United States. Moreover, established oncogenes such as K-RAS and c-MYC, which had been previously demonstrated to induce intracellular ROS56,57, have been recently shown to stabilize Nrf258. Proliferator-Activated Receptor Attenuates Hypertensive Vascular Remodeling by Protecting Vascular Smooth Muscle Cells from Angiotensin II-Induced ROS Production" Antioxidants 11, no. If you want to reproduce the whole article Chem. Oncol. 2001 Nov 15;55(4):236-48. doi: 10.1002/jemt.1173. DNA oxidation as triggered by H3K9me2 demethylation drives estrogen-induced gene expression. Since Fe(II) catalyzes the Fenton reaction to produce the free radical OH* from hydrogen peroxide, its upregulation presents a paradox: Nrf2 also boosts the expression of the genes encoding several components of the ferritin complex that detoxifies Fe(II) by converting it to Fe(III) and then stores it22. Among these, bortezomib is a proteasome inhibitor that induces ROS and ER stress in head and neck squamous cell carcinoma cells112, and celecoxib, a nonsteroidal anti-inflammatory drug, aggravates ER stress and induces apoptosis by altering the Bax/Bcl-2 ratio and increasing ROS in prostate cancer cells113. Atmospheric gas plasma-induced ROS production activates TNF-ASK1 pathway for the induction of melanoma cancer cell apoptosis. & Pollard, J. W. Microenvironmental regulation of metastasis. Cardiol. Misale, S. et al. Epub 2009 Feb 26. Clin Res Hepatol Gastroenterol 40(4):487493, Senbanjo LT, Chellaiah MA (2017) CD44: a multifunctional cell surface adhesion receptor is a regulator of progression and metastasis of Cancer cells. Macrophages (abbreviated as M , M or MP) ( Greek: large eaters, from Greek ( makrs) = large, ( phagein) = to eat) are a type of white blood cell of the immune system that engulfs and digests pathogens, such as cancer cells, microbes, cellular debris, and foreign substances, which do not have proteins that are . PubMed Ann Transl Med 4(24):518, Cosentino C et al (2011) ATM activates the pentose phosphate pathway promoting anti-oxidant defence and DNA repair. Science 350, 13911396 (2015). Reactive oxygen species are essential for autophagy and specifically regulate the activity of Atg4. Under normal conditions, Nrf2 is degraded through its interaction with Kelch-like ECH-associated protein 1 (Keap1), whereas under oxidative stress conditions, Keap1 is oxidized and Nrf2 is translocated to the nucleus, where it induces the expression of several genes19. Hydrogen peroxide (H 2 O 2 ), a type of ROS, promotes pro-tumorigenic signaling by mediating the cysteine oxidation of target proteins to alter their function. Zhao Y, Hu J, Yang SS, Zhong J, Liu J, Wang S, Jiao Y, Jiang F, Zhai R, Ren B, Cong H, Zhu Y, Han F, Zhang J, Xu Y, Huang Z, Zhang S, Yang F. Nat Commun. Steeg, P. S. Targeting metastasis. Epub 2017 Jan 11. CAFs can also promote cancer growth and invasiveness, and both CAFS and ROS are linked through the increases in ROS-generated CAFs to which most cancers respond by increasing the expression of antioxidant genes52,53,54 (Fig. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. Moderate increases of ROS contribute to several pathologic conditions, among which are tumor promotion and progression, as they are involved in different signaling pathways and induce DNA mutation. J Clin Invest 122(5):18491868, Chang W-W et al (2008) Expression of Globo H and SSEA3 in breast cancer stem cells and the involvement of fucosyl transferases 1 and 2 in Globo H synthesis. The xc-cystine/glutamate antiporter as a potential therapeutic target for small-cell lung cancer: use of sulfasalazine. 2012 Jun 1;16(11):1295-322. doi: 10.1089/ars.2011.4414. The pivotal redox-sensitive transcription factor is nuclear factor erythroid 2-related factor 2 (Nrf2)19, recognized as the leading transcription factor driving the antioxidant response in cancer cells. J Biol Chem 277(23):2033620342, Li JJ et al (2006) Role of oxidative stress in the apoptosis of hepatocellular carcinoma induced by combination of arsenic trioxide and ascorbic acid 1. Clin. Wang, H. et al. Rep. 6, 33222 (2016). Copyright Clearance Center request page. Adv Drug Deliv Rev. B. et al. Finally, we provide evidence that nutraceuticals derived from Mother Nature are highly effective in eliminating cancer cells. Rev. Rev. 2022 Jun 22;14(7):1323. doi: 10.3390/pharmaceutics14071323. It is now well accepted that moderate levels of ROS are required for several cellular functions, including gene expression. All these reports have contributed to the cementing of the existence of cancer stem cells and the extensive role they play in cancer and its metastasis. Buytaert, E., Dewaele, M. & Agostinis, P. Molecular effectors of multiple cell death pathways initiated by photodynamic therapy. Here, we report a newly discovered nexus between changes in cancer metabolism and chromatin remodeling permissive to cell plasticity acquisition. Among the targets of p53 activity are sestrins (sestrin 1 and 2) that induce the activity of peroxiredoxins, increasing the impact of the cellular antioxidant array26. In the present study, we investigate the production of intracellular Reactive Oxygen Species (ROS) as a mechanism to induce cell death under these conditions. Oncogenomics, Elsevier:7787, Ito K et al (2008) PML targeting eradicates quiescent leukaemia-initiating cells. Perillo, B., Di Donato, M., Pezone, A. et al. Trends Genet. It has been reported that by inhibiting phosphorylation of serine 10 in this pathway, breast cancer cells simultaneously challenged with estradiol show an overproduction of ROS, with increased oxidation of the DNA that overwhelms the repair apparatus and triggers PCD in a great percentage of these cells144 (Fig. Moreover, the use of drugs affecting mitochondria, where more than one-half of all ROS are generated, represents a suitable approach to induce oxidative stress and PCD in cancer cells109: gamitrinib, an inhibitor of heat shock protein 90 (HSP90), induces a dramatic collapse of mitochondria in prostate cancer cells110, while ARQ 501 (a quinone derivative) and STA-4783 (a copper chelator) increase ROS through leakage in the electron transport chain and have beneficial effects in patients with solid tumors and pancreatic adenocarcinoma111. Sobhakumari, A. et al. 8, 579591 (2009). Natl Acad. 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Proc Natl Acad Sci 100(7):39833988, CrossRef Gorrini, C. et al. iglesias@ugr.es. Epub 2013 Aug 24. Lingappan, K. NF-kB in oxidative stress. Perillo, B. et al. Biosens Bioelectron 80:491496, Zhao T et al (2014) HIF-1-mediated metabolic reprogramming reduces ROS levels and facilitates the metastatic colonization of cancers in lungs. However, it has also been observed that hormone-induced phosphorylation of serine 10 in H3 histone (H3S10) prevents the rapid remethylation of the preceding lysine, serving as the metronome of the process and giving the DNA damage repair system enough time to eliminate the oxidized nucleotides from nearby DNA143. variouscatechins used Toxins2016,8,372of16 . ):30253029, Behbod F, Vivanco MD ( 2015 ) drug efflux pumps proapoptotic.. Death and sustained JNK activation by inhibiting MAP kinase phosphatases targeted locus: mechanism of allele methylation polymorphism adult cells. 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