Publicación: Evaluación de la eficacia terapéutica de sulforafano y docetaxel sobre un modelo in vitro de cáncer de próstata
dc.contributor.advisor | Espitia Pérez, Pedro Juan | spa |
dc.contributor.author | Peñata Taborda, Ana Marcela | |
dc.date.accessioned | 2023-01-28T01:59:12Z | |
dc.date.available | 2023-01-28T01:59:12Z | |
dc.date.issued | 2023-01-27 | |
dc.description.abstract | El cáncer de próstata (CP) es la quinta causa de muerte a nivel mundial y la segunda neoplasia maligna mayormente diagnosticada en hombres, siendo la principal causa de muerte en la población masculina colombiana. Las células cancerosas de próstata muestran una actividad metabólica y redox anormal, y la evidencia emergente indica que el comportamiento de este tipo de cáncer se ha relacionado con características tumorales agresivas como la quimiorresistencia, invasividad y potencial metastásico, entre otras. Además, los medicamentos utilizados en oncología clínica tienen índices terapéuticos estrechos con toxicidad adversa, que a menudo implica daño oxidativo en los tejidos normales. El Docetaxel (DCT) es un fármaco antineoplásico, utilizado para el tratamiento de CP, su citotoxicidad y emergente resistencia han limitado su eficacia. Las terapias de combinación tienen el propósito de sensibilizar los tumores y proteger tejidos no afectados lo aumenta el índice terapéutico. El Sulforafano (SFN), es un fitoquímico de amplio interés clínico, debido a sus propiedades anticancerígenas y efectos promisorios en terapias de combinación. En consecuencia, la presente investigación tuvo como objetivo evaluar la eficacia terapeutica de SFN y DCT sobre un modelo in vitro de CP de diferente sensibilidad a quimioterapia como estrategia antitumoral. En esta investigación de tipo experimental, se usaron líneas celulares de CP con diferentes niveles de tumorigenicidad y quimioresistencia, así como la contraparte no tumoral, de modo que ofrecieran diferentes características redox y metabólicas. | spa |
dc.description.abstract | Prostate cancer (PC) is the fifth leading cause of death worldwide and the second most diagnosed malignancy in men, being the leading cause of death in the Colombian male population. Prostate cancer cells show abnormal metabolic and redox activity, and emerging evidence indicates that the behavior of this type of cancer has been related to aggressive tumor characteristics such as chemoresistance, invasiveness, and metastatic potential, among others. In addition, drugs used in clinical oncology have narrow therapeutic indexes with adverse toxicity, often involving oxidative damage to normal tissues. Docetaxel (DCT) is an antineoplastic drug used to treat PC; its cytotoxicity and emerging resistance have limited its efficacy. Combination therapies are intended to sensitize tumors and protect unaffected tissues, which increases the therapeutic index. Sulforaphane (SFN) is a phytochemical of broad clinical interest due to its anticancer properties and promising effects in combination therapies. Consequently, the present research aimed to evaluate the therapeutic efficacy of SFN and DCT on an in vitro model of PC with different sensitivity to chemotherapy as an antitumor strategy. In this experimental-type investigation, PC cell lines with different levels of tumorigenicity and chemoresistance, as well as the non-tumorigenic counterpart, were used to offer different redox and metabolic characteristics. | eng |
dc.description.degreelevel | Maestría | spa |
dc.description.degreename | Magíster en Biotecnología | spa |
dc.description.modality | Trabajos de Investigación y/o Extensión | spa |
dc.description.tableofcontents | LISTA DE FIGURAS ................................................................ 7 | spa |
dc.description.tableofcontents | LISTA DE TABLAS........................................................................... 8 | spa |
dc.description.tableofcontents | LISTA DE ANEXOS .............................................................................. 8 | spa |
dc.description.tableofcontents | RESUMEN................................................................................ 9 | spa |
dc.description.tableofcontents | ABSTRACT ................................................................................ 11 | spa |
dc.description.tableofcontents | INTRODUCCIÓN................................................................... 13 | spa |
dc.description.tableofcontents | MARCO TEÓRICO Y ANTECEDENTES ............................................. 17 | spa |
dc.description.tableofcontents | Etiología y patología del cáncer de próstata ...................................17 | spa |
dc.description.tableofcontents | La quimioterapia del cáncer de próstata .......................................19 | spa |
dc.description.tableofcontents | Estrés Oxidativo y el cáncer de próstata .................................20 | spa |
dc.description.tableofcontents | Metabolismo del cáncer de próstata...........................................22 | spa |
dc.description.tableofcontents | Fitoquímicos en el tratamiento del cáncer de próstata: Sulforafano..............25 | spa |
dc.description.tableofcontents | OBJETIVOS......................................................................................... 27 | spa |
dc.description.tableofcontents | Objetivo .......................................................................................27 | spa |
dc.description.tableofcontents | Objetivos específicos.............................................................27 | spa |
dc.description.tableofcontents | MATERIALES Y MÉTODOS...................................................... 28 | spa |
dc.description.tableofcontents | Área y tipo de estudio ..............................................................28 | spa |
dc.description.tableofcontents | Cultivos celulares...............................................................28 | spa |
dc.description.tableofcontents | Ensayo de viabilidad por Cristal violeta ..........................29 | spa |
dc.description.tableofcontents | Ensayo de MTT [bromuro de 3- (4,5-dimetiltiazol-2-il) -2,5-difeniltetrazolio)] .............30 | spa |
dc.description.tableofcontents | Detección y caracterización de la apoptosis .........................................31 | spa |
dc.description.tableofcontents | Ensayo de muerte celular por Anexina V ...................................31 | spa |
dc.description.tableofcontents | Actividad caspasas 3, 8 y 9.............................................................31 | spa |
dc.description.tableofcontents | Evaluación de los efectos combinados SFN y DCT mediante análisis de isobologramas ............32 | spa |
dc.description.tableofcontents | Caracterización de los tratamientos combinados SFN y DCT sobre el estado redox y metabólico.....................................................................32 | spa |
dc.description.tableofcontents | Consumo de glucosa y fermentación láctica......................................32 | spa |
dc.description.tableofcontents | Caracterización redox .......................................................34 | spa |
dc.description.tableofcontents | Determinación de ROS intracelular.....................................34 | spa |
dc.description.tableofcontents | Masa mitocondrial relativa ...........................................34 | spa |
dc.description.tableofcontents | Determinación de GSH, GSSG y la relación GSH/GSSG................35 | spa |
dc.description.tableofcontents | Niveles de expresión (ARNm) de genes regulados por Nrf2, y HIF-1.............................36 | spa |
dc.description.tableofcontents | Análisis estadístico ..............................................................36 | spa |
dc.description.tableofcontents | RESULTADOS ..................................................................... 37 | spa |
dc.description.tableofcontents | DISCUSIÓN............................................................................ 51 | spa |
dc.description.tableofcontents | CONCLUSIONES......................................................................... 59 | spa |
dc.description.tableofcontents | REFERENCIAS BIBLIOGRAFICAS ........................................................ 60 | spa |
dc.description.tableofcontents | ANEXOS........................................................................................ 70 | spa |
dc.format.mimetype | application/pdf | spa |
dc.identifier.uri | https://repositorio.unicordoba.edu.co/handle/ucordoba/6959 | |
dc.language.iso | spa | spa |
dc.publisher | Universidad de Córdoba | spa |
dc.publisher.faculty | Facultad de Ciencias Básicas | spa |
dc.publisher.place | Montería, Córdoba, Colombia | spa |
dc.publisher.program | Química | spa |
dc.rights | Copyright Universidad de Córdoba, 2023 | spa |
dc.rights.accessrights | info:eu-repo/semantics/openAccess | spa |
dc.rights.creativecommons | Atribución-NoComercial-SinDerivadas 4.0 Internacional (CC BY-NC-ND 4.0) | spa |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/4.0/ | spa |
dc.subject.keywords | Chemoresistance | eng |
dc.subject.keywords | Combination therapy | eng |
dc.subject.keywords | Sulforaphane | eng |
dc.subject.keywords | Glycolysis | eng |
dc.subject.keywords | Redox metabolism | eng |
dc.subject.proposal | Quimioresistencia | spa |
dc.subject.proposal | Sulforafano | spa |
dc.subject.proposal | Terapia de combinación | spa |
dc.subject.proposal | Glucolisis | spa |
dc.subject.proposal | Metabolismo redox | spa |
dc.title | Evaluación de la eficacia terapéutica de sulforafano y docetaxel sobre un modelo in vitro de cáncer de próstata | spa |
dc.type | Trabajo de grado - Maestría | spa |
dc.type.coar | http://purl.org/coar/resource_type/c_bdcc | spa |
dc.type.content | Text | spa |
dc.type.driver | info:eu-repo/semantics/masterThesis | spa |
dc.type.redcol | https://purl.org/redcol/resource_type/TM | spa |
dc.type.version | info:eu-repo/semantics/submittedVersion | spa |
dcterms.references | [1] Bray F, Laversanne M, Weiderpass E, Soerjomataram I. The ever‐increasing importance of cancer as a leading cause of premature death worldwide. Cancer 2021;127:3029–30. https://doi.org/10.1002/cncr.33587 | spa |
dcterms.references | [2] Sung H, Ferlay J, Siegel RL, Laversanne M, Soerjomataram I, Jemal A, et al. Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries. CA A Cancer J Clin 2021;71:209–49. https://doi.org/10.3322/caac.21660 | spa |
dcterms.references | [3] Culp MB, Soerjomataram I, Efstathiou JA, Bray F, Jemal A. Recent Global Patterns in Prostate Cancer Incidence and Mortality Rates. European Urology 2020;77:38–52. https://doi.org/10.1016/j.eururo.2019.08.005 | spa |
dcterms.references | [4] World Health Organization. Globocan Colombia [Internet]. Vol. 380. 2018. Available from: http://www.consultorsalud.com/sites/consultorsalud/files/170-colombia-fact-sheets.pdf | spa |
dcterms.references | [5] Instituto Nacional de Cancerología. Infocancer, 2021 [Internet]. Información de Cancer en Colombia. 2021 [cited 2021 Dec 7]. p. 1–3. Available from: https://www.infocancer.co/portal/#!/filtro_mortalidad/ | spa |
dcterms.references | [6] Pardo Ramos C, Vries E de, Buitrago Reyes LA, Gamboa Garay O. Atlas de mortalidad por cáncer en Colombia. Cuarta edición. Bogotá D.C., Colombia: Instituto Nacional de Cancerología - ESE; 2017. | spa |
dcterms.references | [7] Szakács G, Paterson JK, Ludwig JA, Booth-Genthe C, Gottesman MM. Targeting multidrug resistance in cancer. Nat Rev Drug Discov 2006;5:219–34. https://doi.org/10.1038/nrd1984 | spa |
dcterms.references | [8] Gillessen S, Omlin A, Attard G, de Bono JS, Efstathiou E, Fizazi K, et al. Management of patients with advanced prostate cancer: recommendations of the St Gallen Advanced Prostate Cancer Consensus Conference (APCCC) 2015. Annals of Oncology 2015;26:1589–604. https://doi.org/10.1093/annonc/mdv257 | spa |
dcterms.references | [9] Tsaur I, Heidegger I, Kretschmer A, Borgmann H, Gandaglia G, Briganti A, et al. Aggressive variants of prostate cancer Are we ready to apply specific treatment right now? Cancer Treatment Reviews 2019;75:20–6. https://doi.org/10.1016/j.ctrv.2019.03.001 | spa |
dcterms.references | [10] Gravis G. Systemic treatment for metastatic prostate cancer. Asian Journal of Urology 2019;6:162–8. https://doi.org/10.1016/j.ajur.2019.02.002 | spa |
dcterms.references | [11] Seng SM, Tsao C-K, Galsky MD, Oh WK. Cytotoxic chemotherapy for castration resistant prostate cancer: 2010 and beyond. Drug Discovery Today: Therapeutic Strategies 2010;7:17–22. https://doi.org/10.1016/j.ddstr.2011.02.001 | spa |
dcterms.references | [12] Ho M, Mackey J. Presentation and management of docetaxel-related adverse effects in patients with breast cancer. CMAR 2014:253. https://doi.org/10.2147/CMAR.S40601 | spa |
dcterms.references | [13] Al-Batran S-E, Hozaeel W, Tauchert FK, Hofheinz R-D, Hinke A, Windemuth-Kieselbach C, et al. The impact of docetaxel-related toxicities on health-related quality of life in patients with metastatic cancer (QoliTax). Annals of Oncology 2015;26:1244–8. https://doi.org/10.1093/annonc/mdv129 | spa |
dcterms.references | [14] Alimbetov D, Askarova S, Umbayev B, Davis T, Kipling D. Pharmacological Targeting of Cell Cycle, Apoptotic and Cell Adhesion Signaling Pathways Implicated in Chemoresistance of Cancer Cells. IJMS 2018;19:1690. https://doi.org/10.3390/ijms19061690 | spa |
dcterms.references | [15] Negrette-Guzmán M. Combinations of the antioxidants sulforaphane or curcumin and the conventional antineoplastics cisplatin or doxorubicin as prospects for anticancer chemotherapy. European Journal of Pharmacology 2019;859:172513. https://doi.org/10.1016/j.ejphar.2019.172513 | spa |
dcterms.references | [16] Negrette-Guzmán M, Huerta-Yepez S, Tapia E, Pedraza-Chaverri J. Modulation of mitochondrial functions by the indirect antioxidant sulforaphane: A seemingly contradictory dual role and an integrative hypothesis. Free Radical Biology and Medicine 2013;65:1078–89. https://doi.org/10.1016/j.freeradbiomed.2013.08.182 | spa |
dcterms.references | [17] Kamal MM, Akter S, Lin C-N, Nazzal S. Sulforaphane as an anticancer molecule: mechanisms of action, synergistic effects, enhancement of drug safety, and delivery systems. Arch Pharm Res 2020;43:371–84. https://doi.org/10.1007/s12272-020-01225-2 | spa |
dcterms.references | [18] Juge N, Mithen RF, Traka M. Molecular basis for chemoprevention by sulforaphane: a comprehensive review. Cell Mol Life Sci 2007;64:1105–27. https://doi.org/10.1007/s00018-007- 6484-5 | spa |
dcterms.references | [19] Kaiser AE, Baniasadi M, Giansiracusa D, Giansiracusa M, Garcia M, Fryda Z, et al. Sulforaphane: A Broccoli Bioactive Phytocompound with Cancer Preventive Potential. Cancers 2021;13:4796. https://doi.org/10.3390/cancers13194796 | spa |
dcterms.references | [20] Kahroba H, Shirmohamadi M, Hejazi MS, Samadi N. The Role of Nrf2 signaling in cancer stem cells: From stemness and self-renewal to tumorigenesis and chemoresistance. Life Sciences 2019;239:116986. https://doi.org/10.1016/j.lfs.2019.116986 | spa |
dcterms.references | [21] Piantadosi CA, Carraway MS, Babiker A, Suliman HB. Heme Oxygenase-1 Regulates Cardiac Mitochondrial Biogenesis via Nrf2-Mediated Transcriptional Control of Nuclear Respiratory Factor 1. Circulation Research 2008;103:1232–40. https://doi.org/10.1161/01.RES.0000338597.71702.ad. | spa |
dcterms.references | [22] MacGarvey NC, Suliman HB, Bartz RR, Fu P, Withers CM, Welty-Wolf KE, et al. Activation of Mitochondrial Biogenesis by Heme Oxygenase-1–mediated NF-E2–related Factor-2 Induction Rescues Mice from Lethal Staphylococcus aureus Sepsis. Am J Respir Crit Care Med 2012;185:851– 61. https://doi.org/10.1164/rccm.201106-1152OC | spa |
dcterms.references | [23] Negrette-Guzmán M, Huerta-Yepez S, Vega MI, León-Contreras JC, Hernández-Pando R, Medina-Campos ON, et al. Sulforaphane induces differential modulation of mitochondrial biogenesis and dynamics in normal cells and tumor cells. Food and Chemical Toxicology 2017;100:90–102. https://doi.org/10.1016/j.fct.2016.12.020. | spa |
dcterms.references | [24] Monsef N, Helczynski L, Lundwall A, Påhlman S, Anders-Bjartell. Localization of immunoreactive HIF-1α and HIF-2α in neuroendocrine cells of both benign and malignant prostate glands. Prostate 2007;67:1219–29. https://doi.org/10.1002/pros.20594. | spa |
dcterms.references | [25] Kim DH, Sung B, Kang YJ, Hwang SY, Kim MJ, Yoon J-H, et al. Sulforaphane inhibits hypoxia-induced HIF-1α and VEGF expression and migration of human colon cancer cells. International Journal of Oncology 2015;47:2226–32. https://doi.org/10.3892/ijo.2015.3200. | spa |
dcterms.references | [26] Yao H, Wang H, Zhang Z, Jiang B, Luo J, Shi X. Sulforaphane inhibited expression of hypoxia‐ inducible factor‐1α in human tongue squamous cancer cells and prostate cancer cells. Int J Cancer 2008;123:1255–61. https://doi.org/10.1002/ijc.23647. | spa |
dcterms.references | [27] Yagishita Y, Fahey JW, Dinkova-Kostova AT, Kensler TW. Broccoli or Sulforaphane: Is It the Source or Dose That Matters? Molecules 2019;24:3593. https://doi.org/10.3390/molecules24193593. | spa |
dcterms.references | [28] Kallifatidis G, Labsch S, Rausch V, Mattern J, Gladkich J, Moldenhauer G, et al. Sulforaphane Increases Drug-mediated Cytotoxicity Toward Cancer Stem-like Cells of Pancreas and Prostate. Molecular Therapy 2011;19:188–95. https://doi.org/10.1038/mt.2010.216. | spa |
dcterms.references | [29] Burnett JP, Shah RB, Paholak HJ, McDermott SP, Tsume Y, Wicha MW, et al. Abstract 4076: Combination of docetaxel with sulforaphane synergistically inhibits triple negative breast cancer and cancer stem cells. Cancer Research 2015;75:4076–4076. https://doi.org/10.1158/1538- 7445.AM2015-4076. | spa |
dcterms.references | [30] Burnett JP, Lim G, Li Y, Shah RB, Lim R, Paholak HJ, et al. Sulforaphane enhances the anticancer activity of taxanes against triple negative breast cancer by killing cancer stem cells. Cancer Letters 2017;394:52–64. https://doi.org/10.1016/j.canlet.2017.02.023 | spa |
dcterms.references | [31] Cooperberg MR, Erho N, Chan JM, Feng FY, Fishbane N, Zhao SG, et al. The Diverse Genomic Landscape of Clinically Low-risk Prostate Cancer. European Urology 2018;74:444–52. https://doi.org/10.1016/j.eururo.2018.05.014. | spa |
dcterms.references | [32] Demichelis F, Stanford JL. Genetic predisposition to prostate cancer: Update and future perspectives. Urologic Oncology: Seminars and Original Investigations 2015;33:75–84. https://doi.org/10.1016/j.urolonc.2014.04.021 | spa |
dcterms.references | [33] Malik SS, Batool R, Masood N, Yasmin A. Risk factors for prostate cancer: A multifactorial case-control study. Current Problems in Cancer 2018;42:337–43. https://doi.org/10.1016/j.currproblcancer.2018.01.014. | spa |
dcterms.references | [34] Leitzmann M, Rohrmann S. Risk factors for the onset of prostatic cancer: age, location, and behavioral correlates. CLEP 2012:1. https://doi.org/10.2147/CLEP.S16747. | spa |
dcterms.references | [35] Zhang X, Zhou G, Sun B, Zhao G, Liu D, Sun J, et al. Impact of obesity upon prostate cancer associated mortality: A meta-analysis of 17 cohort studies. Oncology Letters 2015;9:1307–12. https://doi.org/10.3892/ol.2014.2841. | spa |
dcterms.references | [36] Freeland J, Crowell PD, Giafaglione JM, Boutros PC, Goldstein AS. Aging of the progenitor cells that initiate prostate cancer. Cancer Letters 2021;515:28–35. https://doi.org/10.1016/j.canlet.2021.05.014. | spa |
dcterms.references | [37] Yizhak K, Aguet F, Kim J, Hess JM, Kübler K, Grimsby J, et al. RNA sequence analysis reveals macroscopic somatic clonal expansion across normal tissues. Science 2019;364:eaaw0726. https://doi.org/10.1126/science.aaw0726 | spa |
dcterms.references | [38] Rebbeck TR, Devesa SS, Chang B-L, Bunker CH, Cheng I, Cooney K, et al. Global Patterns of Prostate Cancer Incidence, Aggressiveness, and Mortality in Men of African Descent. Prostate Cancer 2013;2013:1–12. https://doi.org/10.1155/2013/560857. | spa |
dcterms.references | [39] Coughlin SS, Vernon M, Klaassen Z, Tingen MS, Cortes JE. Knowledge of prostate cancer among African American men: A systematic review. The Prostate 2021;81:202–13. https://doi.org/10.1002/pros.24097. | spa |
dcterms.references | [40] Harris WP, Mostaghel EA, Nelson PS, Montgomery B. Androgen deprivation therapy: progress in understanding mechanisms of resistance and optimizing androgen depletion. Nat Rev Urol 2009;6:76–85. https://doi.org/10.1038/ncpuro1296 | spa |
dcterms.references | [41] Nelson AW, Tilley WD, Neal DE, Carroll JS. Estrogen receptor beta in prostate cancer: friend or foe? Endocrine-Related Cancer 2014;21:T219–34. https://doi.org/10.1530/ERC-13-0508. | spa |
dcterms.references | [42] Nelson AW, Shah N. Prostate cancer. Surgery (Oxford) 2019;37:500–7. https://doi.org/10.1016/j.mpsur.2019.07.006 | spa |
dcterms.references | [43] Vlajnic T, Bubendorf L. Molecular pathology of prostate cancer: a practical approach. Pathology 2021;53:36–43. https://doi.org/10.1016/j.pathol.2020.10.003 | spa |
dcterms.references | [44] Gyawali B, Koomulli-Parambil S, Iddawela M. Continuous versus intermittent docetaxel for metastatic castration resistant prostate cancer. Critical Reviews in Oncology/Hematology 2016;102:118–24. https://doi.org/10.1016/j.critrevonc.2016.04.014 | spa |
dcterms.references | [45] Gillessen S, Omlin A, Attard G, de Bono JS, Efstathiou E, Fizazi K, et al. Management of patients with advanced prostate cancer: recommendations of the St Gallen Advanced Prostate Cancer Consensus Conference (APCCC) 2015. Annals of Oncology 2015;26:1589–604. https://doi.org/10.1093/annonc/mdv257 | spa |
dcterms.references | [46] Saad F, Miller K. Treatment options in castration-resistant prostate cancer: Current therapies and emerging docetaxel-based regimens. Urologic Oncology: Seminars and Original Investigations 2014;32:70–9. https://doi.org/10.1016/j.urolonc.2013.01.005 | spa |
dcterms.references | [47] Nieuweboer AJM, de Morrée ES, de Graan A-JM, Sparreboom A, de Wit R, Mathijssen RHJ. Inter-patient variability in docetaxel pharmacokinetics: A review. Cancer Treatment Reviews 2015;41:605–13. https://doi.org/10.1016/j.ctrv.2015.04.012 | spa |
dcterms.references | [48] Kroon J, Kooijman S, Cho N-J, Storm G, van der Pluijm G. Improving Taxane-Based Chemotherapy in Castration-Resistant Prostate Cancer. Trends in Pharmacological Sciences 2016;37:451–62. https://doi.org/10.1016/j.tips.2016.03.003 | spa |
dcterms.references | [49] Zu S, Ma W, Xiao P, Cui Y, Ma T, Zhou C, et al. Evaluation of Docetaxel-Sensitive and Docetaxel-Resistant Proteomes in PC-3 Cells. Urol Int 2015;95:114–9. https://doi.org/10.1159/000351263 | spa |
dcterms.references | [50] Thadani-Mulero M, Portella L, Sun S, Sung M, Matov A, Vessella RL, et al. Androgen Receptor Splice Variants Determine Taxane Sensitivity in Prostate Cancer. Cancer Res 2014;74:2270–82. https://doi.org/10.1158/0008-5472.CAN-13-2876. | spa |
dcterms.references | [51] Mahon KL, Henshall SM, Sutherland RL, Horvath LG. Pathways of chemotherapy resistance in castration-resistant prostate cancer. Endocrine-Related Cancer 2011;18:R103–23. https://doi.org/10.1530/ERC-10-0343 | spa |
dcterms.references | [52] Baker J, Ajani J, Scotté F, Winther D, Martin M, Aapro MS, et al. Docetaxel-related side effects and their management. European Journal of Oncology Nursing 2009;13:49–59. https://doi.org/10.1016/j.ejon.2008.10.003 | spa |
dcterms.references | [53] Valko M, Leibfritz D, Moncol J, Cronin MTD, Mazur M, Telser J. Free radicals and antioxidants in normal physiological functions and human disease. The International Journal of Biochemistry & Cell Biology 2007;39:44–84. https://doi.org/10.1016/j.biocel.2006.07.001 | spa |
dcterms.references | [54] Circu ML, Aw TY. Reactive oxygen species, cellular redox systems, and apoptosis. Free Radical Biology and Medicine 2010;48:749–62. https://doi.org/10.1016/j.freeradbiomed.2009.12.022 | spa |
dcterms.references | [55] Boese AC, Kang S. Mitochondrial metabolism-mediated redox regulation in cancer progression. Redox Biology 2021;42:101870. https://doi.org/10.1016/j.redox.2021.101870 | spa |
dcterms.references | [56] Kim E-K, Jang M, Song M-J, Kim D, Kim Y, Jang HH. Redox-Mediated Mechanism of Chemoresistance in Cancer Cells. Antioxidants 2019;8:471. https://doi.org/10.3390/antiox8100471 | spa |
dcterms.references | [57] Chun K-S, Raut PK, Kim D-H, Surh Y-J. Role of chemopreventive phytochemicals in NRF2- mediated redox homeostasis in humans. Free Radical Biology and Medicine 2021;172:699–715. https://doi.org/10.1016/j.freeradbiomed.2021.06.031 | spa |
dcterms.references | [58] Bai X, Chen Y, Hou X, Huang M, Jin J. Emerging role of NRF2 in chemoresistance by regulating drug-metabolizing enzymes and efflux transporters. Drug Metabolism Reviews 2016;48:541–67. https://doi.org/10.1080/03602532.2016.1197239 | spa |
dcterms.references | [59] Vander Heiden MG, DeBerardinis RJ. Understanding the Intersections between Metabolism and Cancer Biology. Cell 2017;168:657–69. https://doi.org/10.1016/j.cell.2016.12.039 | spa |
dcterms.references | [60] Gonzalez-Menendez P, Hevia D, Mayo JC, Sainz RM. The dark side of glucose transporters in prostate cancer: Are they a new feature to characterize carcinomas? The role of GLUT transporters in prostate cancer. Int J Cancer 2018;142:2414–24. https://doi.org/10.1002/ijc.31165 | spa |
dcterms.references | [61] Pavlova NN, Thompson CB. The Emerging Hallmarks of Cancer Metabolism. Cell Metabolism 2016;23:27–47. https://doi.org/10.1016/j.cmet.2015.12.006 | spa |
dcterms.references | [62] Ghanavat M, Shahrouzian M, Deris Zayeri Z, Banihashemi S, Kazemi SM, Saki N. Digging deeper through glucose metabolism and its regulators in cancer and metastasis. Life Sciences 2021;264:118603. https://doi.org/10.1016/j.lfs.2020.118603 | spa |
dcterms.references | [63] Singh D, Arora R, Kaur P, Singh B, Mannan R, Arora S. Overexpression of hypoxia-inducible factor and metabolic pathways: possible targets of cancer. Cell Biosci 2017;7:62. https://doi.org/10.1186/s13578-017-0190-2 | spa |
dcterms.references | [64] Dengler VL, Galbraith MD, Espinosa JM. Transcriptional regulation by hypoxia inducible factors. Critical Reviews in Biochemistry and Molecular Biology 2014;49:1–15. https://doi.org/10.3109/10409238.2013.838205 | spa |
dcterms.references | [65] Tsui K-H, Chung L-C, Wang S-W, Feng T-H, Chang P-L, Juang H-H. Hypoxia upregulates the gene expression of mitochondrial aconitase in prostate carcinoma cells. Journal of Molecular Endocrinology 2013;51:131–41. https://doi.org/10.1530/JME-13-0090 | spa |
dcterms.references | [66] Limón-Pacheco J, Gonsebatt ME. The role of antioxidants and antioxidant-related enzymes in protective responses to environmentally induced oxidative stress. Mutation Research/Genetic Toxicology and Environmental Mutagenesis 2009;674:137–47. https://doi.org/10.1016/j.mrgentox.2008.09.015 | spa |
dcterms.references | [67] Glasauer A, Chandel NS. Targeting antioxidants for cancer therapy. Biochemical Pharmacology 2014;92:90–101. https://doi.org/10.1016/j.bcp.2014.07.017 | spa |
dcterms.references | [68] Chang H-Y, Lin C-W, Yang C-M, Yang C-H. Nrf-2 activator sulforaphane protects retinal cells from oxidative stress-induced retinal injury. Journal of Functional Foods 2020;71:104023. https://doi.org/10.1016/j.jff.2020.104023 | spa |
dcterms.references | [69] Houghton CA. Sulforaphane: Its “Coming of Age” as a Clinically Relevant Nutraceutical in the Prevention and Treatment of Chronic Disease. Oxidative Medicine and Cellular Longevity 2019;2019:1–27. https://doi.org/10.1155/2019/2716870 | spa |
dcterms.references | [70] Zhang Y, Talalay P, Cho CG, Posner GH. A major inducer of anticarcinogenic protective enzymes from broccoli: isolation and elucidation of structure. Proc Natl Acad Sci USA 1992;89:2399–403. https://doi.org/10.1073/pnas.89.6.2399 | spa |
dcterms.references | [71] Wiczk A, Hofman D, Konopa G, Herman-Antosiewicz A. Sulforaphane, a cruciferous vegetable-derived isothiocyanate, inhibits protein synthesis in human prostate cancer cells. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 2012;1823:1295–305. https://doi.org/10.1016/j.bbamcr.2012.05.020 | spa |
dcterms.references | [72] Guerrero-Beltrán CE, Calderón-Oliver M, Pedraza-Chaverri J, Chirino YI. Protective effect of sulforaphane against oxidative stress: Recent advances. Experimental and Toxicologic Pathology 2012;64:503–8. https://doi.org/10.1016/j.etp.2010.11.005 | spa |
dcterms.references | [73] Calabrese V, Cornelius C, Dinkova-Kostova AT, Iavicoli I, Di Paola R, Koverech A, et al. Cellular stress responses, hormetic phytochemicals and vitagenes in aging and longevity. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 2012;1822:753–83. https://doi.org/10.1016/j.bbadis.2011.11.002 | spa |
dcterms.references | [74] Liu Y, Lang F, Yang C. NRF2 in human neoplasm: Cancer biology and potential therapeutic target. Pharmacology & Therapeutics 2021;217:107664. https://doi.org/10.1016/j.pharmthera.2020.107664 | spa |
dcterms.references | [75] Feoktistova M, Geserick P, Leverkus M. Crystal Violet Assay for Determining Viability of Cultured Cells. Cold Spring Harb Protoc 2016;2016:pdb.prot087379. https://doi.org/10.1101/pdb.prot087379 | spa |
dcterms.references | [76] Śliwka L, Wiktorska K, Suchocki P, Milczarek M, Mielczarek S, Lubelska K, et al. The Comparison of MTT and CVS Assays for the Assessment of Anticancer Agent Interactions. PLoS ONE 2016;11:e0155772. https://doi.org/10.1371/journal.pone.0155772 | spa |
dcterms.references | [77] Negrette-Guzmán M, García-Niño WR, Tapia E, Zazueta C, Huerta-Yepez S, León-Contreras JC, et al. Curcumin Attenuates Gentamicin-Induced Kidney Mitochondrial Alterations: Possible Role of a Mitochondrial Biogenesis Mechanism. Evidence-Based Complementary and Alternative Medicine 2015;2015:1–16. https://doi.org/10.1155/2015/917435 | spa |
dcterms.references | [78] Negrette-Guzmán M, Huerta-Yepez S, Medina-Campos ON, Zatarain-Barrón ZL, Hernández Pando R, Torres I, et al. Sulforaphane Attenuates Gentamicin-Induced Nephrotoxicity: Role of Mitochondrial Protection. Evidence-Based Complementary and Alternative Medicine 2013;2013:1– 17. https://doi.org/10.1155/2013/135314 | spa |
dcterms.references | [79] Vega GG, Franco-Cea LA, Huerta-Yepez S, Mayani H, Morrison SL, Bonavida B, et al. Overcoming rituximab drug-resistance by the genetically engineered anti-CD20-hIFN-α fusion protein: Direct cytotoxicity and synergy with chemotherapy. International Journal of Oncology 2015;47:1735–48. https://doi.org/10.3892/ijo.2015.3170 | spa |
dcterms.references | [80] Tallarida RJ. Revisiting the Isobole and Related Quantitative Methods for Assessing Drug Synergism. J Pharmacol Exp Ther 2012;342:2–8. https://doi.org/10.1124/jpet.112.193474 | spa |
dcterms.references | [81] Liu P, Ying Q, Liu H, Yu S, Bu L, Shao L, et al. Curcumin enhances anti‑cancer efficacy of either gemcitabine or docetaxel on pancreatic cancer cells. Oncol Rep 2020. https://doi.org/10.3892/or.2020.7713 | spa |
dcterms.references | [82] Huang R, Pei L, Liu Q, Chen S, Dou H, Shu G, et al. Isobologram Analysis: A Comprehensive Review of Methodology and Current Research. Front Pharmacol 2019;10:1222. https://doi.org/10.3389/fphar.2019.01222 | spa |
dcterms.references | [83] Espitia-Pérez P, Albino SM, Espitia-Pérez L, Brango H, da Rosa H, Kleber Silveira A, et al. Neurobehavioral and oxidative stress alterations following methylmercury and retinyl palmitate co administration in pregnant and lactating rats and their offspring. Neurotoxicology 2018;69:164–80. https://doi.org/10.1016/j.neuro.2018.10.004 | spa |
dcterms.references | [84] Wu W, Peng G, Yang F, Zhang Y, Mu Z, Han X. Sulforaphane has a therapeutic effect in an atopic dermatitis murine model and activates the Nrf2/HO‑1 axis. Mol Med Report 2019. https://doi.org/10.3892/mmr.2019.10405 | spa |
dcterms.references | [85] Dueregger A, Schöpf B, Eder T, Höfer J, Gnaiger E, Aufinger A, et al. Differential Utilization of Dietary Fatty Acids in Benign and Malignant Cells of the Prostate. PLoS ONE 2015;10:e0135704. https://doi.org/10.1371/journal.pone.0135704 | spa |
dcterms.references | [86] Ahmad F, Cherukuri MK, Choyke PL. Metabolic reprogramming in prostate cancer. Br J Cancer 2021;125:1185–96. https://doi.org/10.1038/s41416-021-01435-5 | spa |
dcterms.references | [87] Imran M, Saleem S, Chaudhuri A, Ali J, Baboota S. Docetaxel: An update on its molecular mechanisms, therapeutic trajectory and nanotechnology in the treatment of breast, lung and prostate cancer. Journal of Drug Delivery Science and Technology 2020;60:101959. https://doi.org/10.1016/j.jddst.2020.101959 | spa |
dcterms.references | [88] Rutz J, Thaler S, Maxeiner S, Chun FK-H, Blaheta RA. Sulforaphane Reduces Prostate Cancer Cell Growth and Proliferation In Vitro by Modulating the Cdk-Cyclin Axis and Expression of the CD44 Variants 4, 5, and 7. IJMS 2020;21:8724. https://doi.org/10.3390/ijms21228724 | spa |
dcterms.references | [89] Liang J, Hänsch GM, Hübner K, Samstag Y. Sulforaphane as anticancer agent: A double-edged sword? Tricky balance between effects on tumor cells and immune cells. Advances in Biological Regulation 2019;71:79–87. https://doi.org/10.1016/j.jbior.2018.11.006 | spa |
dcterms.references | [90] Quiros-Gonzalez I, Gonzalez-Menendez P, Mayo JC, Hevia D, Artime-Naveda F, Fernandez Vega S, et al. Androgen-Dependent Prostate Cancer Cells Reprogram Their Metabolic Signature upon GLUT1 Upregulation by Manganese Superoxide Dismutase. Antioxidants (Basel) 2022;11:313. https://doi.org/10.3390/antiox11020313 | spa |
dcterms.references | [91] Shalini S, Dorstyn L, Dawar S, Kumar S. Old, new and emerging functions of caspases. Cell Death Differ 2015;22:526–39. https://doi.org/10.1038/cdd.2014.216 | spa |
dcterms.references | [92] Redza-Dutordoir M, Averill-Bates DA. Activation of apoptosis signalling pathways by reactive oxygen species. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 2016;1863:2977– 92. https://doi.org/10.1016/j.bbamcr.2016.09.012 | spa |
dcterms.references | [93] Ippolito L, Marini A, Cavallini L, Morandi A, Pietrovito L, Pintus G, et al. Metabolic shift toward oxidative phosphorylation in docetaxel resistant prostate cancer cells. Oncotarget 2016;7:61890–904. https://doi.org/10.18632/oncotarget.11301 | spa |
dcterms.references | [94] Chen C-L, Lin C-Y, Kung H-J. Targeting Mitochondrial OXPHOS and Their Regulatory Signals in Prostate Cancers. IJMS 2021;22:13435. https://doi.org/10.3390/ijms222413435 | spa |
dcterms.references | [95] Gonzalez-Menendez P, Hevia D, Alonso-Arias R, Alvarez-Artime A, Rodriguez-Garcia A, Kinet S, et al. GLUT1 protects prostate cancer cells from glucose deprivation-induced oxidative stress. Redox Biology 2018;17:112–27. https://doi.org/10.1016/j.redox.2018.03.017 | spa |
dcterms.references | [96] Xian Z-Y, Liu J-M, Chen Q-K, Chen H-Z, Ye C-J, Xue J, et al. Inhibition of LDHA suppresses tumor progression in prostate cancer. Tumour Biol 2015;36:8093–100. https://doi.org/10.1007/s13277-015-3540-x | spa |
dcterms.references | [97] Rauckhorst AJ, Taylor EB. Mitochondrial pyruvate carrier function and cancer metabolism. Current Opinion in Genetics & Development 2016;38:102–9. https://doi.org/10.1016/j.gde.2016.05.003 | spa |
dcterms.references | [98] Vaz CV, Alves MG, Marques R, Moreira PI, Oliveira PF, Maia CJ, et al. Androgen-responsive and nonresponsive prostate cancer cells present a distinct glycolytic metabolism profile. The International Journal of Biochemistry & Cell Biology 2012;44:2077–84. https://doi.org/10.1016/j.biocel.2012.08.013 | spa |
dcterms.references | [99] Muramatsu H, Sumitomo M, Morinaga S, Kajikawa K, Kobayashi I, Nishikawa G, et al. Targeting lactate dehydrogenase‑A promotes docetaxel‑induced cytotoxicity predominantly in castration‑resistant prostate cancer cells. Oncol Rep 2019. https://doi.org/10.3892/or.2019.7171 | spa |
dcterms.references | [100] Shiota M, Yokomizo A, Naito S. Oxidative stress and androgen receptor signaling in the development and progression of castration-resistant prostate cancer. Free Radical Biology and Medicine 2011;51:1320–8. https://doi.org/10.1016/j.freeradbiomed.2011.07.011 | spa |
dcterms.references | [101] Kong H, Chandel NS. Regulation of redox balance in cancer and T cells. Journal of Biological Chemistry 2018;293:7499–507. https://doi.org/10.1074/jbc.TM117.000257 | spa |
dcterms.references | [102] Foo BJ-A, Eu JQ, Hirpara JL, Pervaiz S. Interplay between Mitochondrial Metabolism and Cellular Redox State Dictates Cancer Cell Survival. Oxidative Medicine and Cellular Longevity 2021;2021:1–20. https://doi.org/10.1155/2021/1341604 | spa |
dcterms.references | [103] Kennedy L, Sandhu JK, Harper M-E, Cuperlovic-Culf M. Role of Glutathione in Cancer: From Mechanisms to Therapies. Biomolecules 2020;10:1429. https://doi.org/10.3390/biom10101429 | spa |
dcterms.references | [104] Lash L, Putt D, Jankovich A. Glutathione Levels and Susceptibility to Chemically Induced Injury in Two Human Prostate Cancer Cell Lines. Molecules 2015;20:10399–414. https://doi.org/10.3390/molecules200610399 | spa |
dcterms.references | [105] Miao Z, Yu F, Ren Y, Yang J. d,l-Sulforaphane Induces ROS-Dependent Apoptosis in Human Gliomablastoma Cells by Inactivating STAT3 Signaling Pathway. IJMS 2017;18:72. https://doi.org/10.3390/ijms18010072 | spa |
dcterms.references | [106] Wang L, Tian Z, Yang Q, Li H, Guan H, Shi B, et al. Sulforaphane inhibits thyroid cancer cell growth and invasiveness through the reactive oxygen species-dependent pathway. Oncotarget 2015;6:25917–31. https://doi.org/10.18632/oncotarget.4542 | spa |
dcterms.references | [107] Xie H, Chun FK-H, Rutz J, Blaheta RA. Sulforaphane Impact on Reactive Oxygen Species (ROS) in Bladder Carcinoma. IJMS 2021;22:5938. https://doi.org/10.3390/ijms22115938 | spa |
dcterms.references | [108] Zhang J, Wang J, Wong YK, Sun X, Chen Y, Wang L, et al. Docetaxel enhances lysosomal function through TFEB activation. Cell Death Dis 2018;9:614. https://doi.org/10.1038/s41419-018- 0571-4 | spa |
dcterms.references | [109] Vyas AR, Hahm E-R, Arlotti JA, Watkins S, Stolz DB, Desai D, et al. Chemoprevention of Prostate Cancer by d , l -Sulforaphane Is Augmented by Pharmacological Inhibition of Autophagy. Cancer Research 2013;73:5985–95. https://doi.org/10.1158/0008-5472.CAN-13-0755 | spa |
dcterms.references | [110] Herman-Antosiewicz A, Johnson DE, Singh SV. Sulforaphane Causes Autophagy to Inhibit Release of Cytochrome c and Apoptosis in Human Prostate Cancer Cells. Cancer Research 2006;66:5828–35. https://doi.org/10.1158/0008-5472.CAN-06-0139 | spa |
dcterms.references | [111] Watson GW, Wickramasekara S, Fang Y, Palomera-Sanchez Z, Maier CS, Williams DE, et al. Analysis of autophagic flux in response to sulforaphane in metastatic prostate cancer cells. Mol Nutr Food Res 2015;59:1954–61. https://doi.org/10.1002/mnfr.201500283 | spa |
dcterms.references | [112] Ashrafizadeh M, Paskeh MDA, Mirzaei S, Gholami MH, Zarrabi A, Hashemi F, et al. Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response. J Exp Clin Cancer Res 2022;41:105. https://doi.org/10.1186/s13046-022-02293-6 | spa |
dcterms.references | [113] Cristofani R, Montagnani Marelli M, Cicardi ME, Fontana F, Marzagalli M, Limonta P, et al. Dual role of autophagy on docetaxel-sensitivity in prostate cancer cells. Cell Death Dis 2018;9:889. https://doi.org/10.1038/s41419-018-0866-5 | spa |
dcterms.references | [114] Benischke A-S, Vasanth S, Miyai T, Katikireddy KR, White T, Chen Y, et al. Activation of mitophagy leads to decline in Mfn2 and loss of mitochondrial mass in Fuchs endothelial corneal dystrophy. Sci Rep 2017;7:6656. https://doi.org/10.1038/s41598-017-06523-2 | spa |
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