hydroxycitrate cancer
2015;3:3. 357, 112122, https://doi.org/10.1016/j.jtbi.2014.04.035 (2014). Diabetes. (New York, N.Y.) 123, 309314 (1956). Google Scholar. By using this website, you agree to our von Kamp, A., Thiele, S., Hdicke, O. Liver problems. (A) H&E staining of representative histological sections after Cre recombinase-encoding adenovirus (Ad-Cre) inhalation . The Long-Term Survival of a Patient With Stage IV Renal Cell Carcinoma Following an Integrative Treatment Approach Including the Intravenous -Lipoic Acid/Low-Dose Naltrexone Protocol. Resveratrol displays anti-inflammatory, anti-oxidant, and anti-angiogenic [63] properties and suppresses development and growth of numerous cancer types in preclinical models, including breast, prostate, colon, and liver. The role of the insulin/IGF system in cancer: lessons learned from clinical trials and the energy balance-cancer link. Caloric Restriction Mimetics Enhance Anticancer Immunosurveillance Here, C and C0 are the vectors of tumor blood concentrations and blood concentrations in metabolites at tumor inlet, respectively (in mM), and m is the vector of concentrations of tumor cells intracellular metabolites (in mM). Cifarelli V, Lashinger LM, Devlin KL, Dunlap SM, Huang J, Kaaks R, Pollak MN, Hursting SD. 2010;2(6):a000109. Balkwill, F. & Mantovani, A. Inflammation and cancer: back to Virchow? CR, a chronic reduction of dietary energy intake by approximately 30% without incurrence of malnutrition, is a broadly effective dietary intervention that significantly decreases adiposity and inflammation and improves metabolic profiles in non-obese humans and rodents [1,2,3,4]. Diabetes. Hyperosmolarity causes inflammation through the methylation of protein phosphatase 2a. While the antitumorigenic effects of CR are well established, the mechanism behind this relationship remains unclear, though it is believed that the tumor suppressive effects are mediated, in part, by enhanced apoptosis within tumors, modulation of systemic signals such as insulin-like growth factor (IGF)-1, insulin, metabolic and inflammatory pathways, as well as by reduced angiogenesis. Similarly, CR also maintains immunological fitness of CD4+ T cells during aging to enhance cancer immunotherapy, specifically OX40-agonist immunotherapy [50]. Google Scholar. Conversely, it is believed to be tumor promoting because established tumors can utilize autophagy to reduce oxidative stress and increase mitochondrial function and metabolism in order to promote survival and overcome stress and low nutrient conditions [25, 26]. Cancer Res. Current and future perspectives in advanced bladder cancer: is there a new standard? Brick by brick: metabolism and tumor cell growth. Epub 2017 Dec 19. doi:10.1126/scitranslmed.aai8700. Clipboard, Search History, and several other advanced features are temporarily unavailable. Differential effects of energy stress on AMPK phosphorylation and apoptosis in experimental brain tumor and normal brain. government site. Cancer Res. Raffaghello L, Safdie F, Bianchi G, Dorff T, Fontana L, Longo VD. Am. 18, 5461, https://doi.org/10.1016/j.gde.2008.02.003 (2008). Google Scholar. Klamt, S., Saez-Rodriguez, J. M.H. Emerging studies are showing the positive effect of using Metformin in cancer therapy26,27,28. ADS Sci. Conventional cancer treatments such as chemotherapy, which mainly focus on disrupting the cell division process, have shown being effective in the attenuation of various cancers but also showing significant limits as well as serious sides effects. CR, fasting, and FMD also reduce pro-inflammatory cytokines in the circulation and in the tumor microenvironment niche, as well as reduced leptin, insulin, IGF-1, and glucose. 2016;32(5):5539. Cancer Prev Res (Phila). Here, our model is first used to simulate the growth of a tumor xenograft implanted to a group of mice. Thazhath SS, Wu T, Bound MJ, Checklin HL, Standfield S, Jones KL, Horowitz M, Rayner CK. Schwartz, L. et al. The metabolic network. -, Mini Rev Med Chem. CR has also been shown to reduce vascularization of tumors [9, 16]. Epub 2010 Oct 8. AMPK activation in response to CR conditions results in increased apoptosis within brain tumors while protecting normal cells from the stress [16, 17]. Nevertheless, hydroxycitrate administration alone does not affect systemic glucose or insulin [67]. Google Scholar. most notably hydroxycitrate, which mimic nutrient deprivation, on autophagy and on the efficacy of immunogenic-cell-death-inducing chemotherapy. Mol. Lourdes Sainero-Alcolado, Judit Liao-Pons, Marie Arsenian-Henriksson, Erez Persi, Miquel Duran-Frigola, Eytan Ruppin, Chandan Seth Nanda, Sharavan Vishaan Venkateswaran, Mariia Yuneva, Elizabeth L. Lieu, Tu Nguyen, Jiyeon Kim, Claudio Tomi-Andrino, Alina Pandele, Dong-Hyun Kim, Selva Rupa Christinal Immanuel, Avinash D. Ghanate, Anu Raghunathan, Tea Pemovska, Johannes W. Bigenzahn, Giulio Superti-Furga, Federica Danzi, Raffaella Pacchiana, Alessandra Fiore, Musalula Sinkala, Nicola Mulder & Darren Patrick Martin, Scientific Reports Biomass synthesis is described as the incorporation of amino acids, intermediate metabolites and palmitic acid. PubMed Halted progression of soft palate cancer in a patient treated with the paleolithic ketogenic diet alone: a 20-months follow-up. Current and future clinical studies will inform on which cancers, and at which stage of the cancer process, CR, fasting, or CR mimetic regimens will prove most effective. In the meantime, to ensure continued support, we are displaying the site without styles In the recent years, cancer research succeeded with sensitive detection methods, targeted drug delivery systems, and the identification of a large set of genes differently expressed. All animals received human care in compliance with the Guide for the Care and Use of Laboratory Animals [DHEW Publication No. Unable to load your collection due to an error, Unable to load your delegates due to an error. Ann N Y Acad Sci. Google Scholar. Warburg, O. wrote the manuscript. Before Int J Obes. Mechanistically, the synergizing effects of the fasting-mimicking diet were associated with increased autophagy in the cancer cells and reduced heme oxygenase-1 (HO-1) in the microenvironment, causing increased circulating CD8+ T cells and reduced Treg cells, and resulting in enhanced immunosurveillance and clearance of tumor cells [41, 47]. Abstract. The site is secure. Membranes (Basel). Appl Physiol Nutr Metab. An abnormal mitochondrial-hypoxia inducible factor-1alpha-Kv channel pathway disrupts oxygen sensing and triggers pulmonary arterial hypertension in fawn hooded rats: similarities to human pulmonary arterial hypertension. Antiangiogenic and proapoptotic effects of dietary restriction on experimental mouse and human brain tumors. This figure has not been published elsewhere. A standardized screening method allow identifying the best drug combinations to asses their effects on cancer cells metabolism and tumor growth25. Pharm. Support Care Cancer. 2011;35(5):71427. ADS Chemosensitization of tumors by resveratrol. 2011;1215:15060. ATP citrate lyase inhibition can suppress tumor cell growth. While the impact of CR on age-related pathologies has been studied most extensively in rodent models, data from human observational and randomized clinical trials demonstrate that CR in non-obese humans results in metabolic and molecular changes similar to those observed in rodent models [5]. Short-Term Fasting Synergizes with Solid Cancer Therapy by Boosting This accelerated glycolysis results in a massive release and accumulation of lactate in the blood stream. Active phase I and II clinical trials are ongoing to determine the effect of combining rapamycin with chemotherapeutic regimens, including gemcitabine for osteosarcoma, cyclophosphamide, dexamethasone in myeloma, and mitoxantrone, etoposide and cytarabine for leukemia. Google Scholar. Phenotypic effects of calorie restriction and insulin-like growth factor-1 treatment on body composition and bone mineral density of C57BL/6 mice: implications for cancer prevention. 2017;8:14063. SBM is supported by a T32 training fellowship from the National Institutes of Health (8T32LM012420-02). Cancer cells utilize acetyl CoA as a synthetic precursor to fuel proliferation and growth [66]; thus, blocking acetyl CoA synthesis is a rational approach to specifically target cancer metabolism. Kroemer, G. & Pouyssegur, J. Tumor cell metabolism: cancers Achilles heel. Furthermore, hydroxycitrate is a potent inducer of autophagy. PloS One 10, e0136815, https://doi.org/10.1371/journal.pone.0136815 (2015). Hydroxycitric Acid: Health Benefits, Side Effects, Uses, Dose - RxList Epub 2022 May 21. CAS Mayorek, N., Naftali-Shani, N. & Grunewald, M. Diclofenac inhibits tumor growth in a murine model of pancreatic cancer by modulation of VEGF levels and arginase activity. Article 2008;14(20):636470. An official website of the United States government. Combining lipoic acid to methylene blue reduces the Warburg effect in CHO cells: From TCA cycle activation to enhancing monoclonal antibody production. This approach to kinetic modeling of tumor growth opens avenues to the identification of new metabolic targets. Scientific Reports (Sci Rep) and S.P. Cold Spring Harb Perspect Biol. 2b). Once glycogen stores are depleted, amino acids and fatty acids are catabolized to generate glucose and ketone bodies, respectively [39]. Despite it not being clear whether administration of CR would support tumor growth in these circumstances, it is thought that transformed cells lack the metabolic adaptability to respond to altered substrate availability, having already invested heavily in metabolic reprograming and thus being more sensitive to increased pressure on ketone metabolism and fatty acid oxidation than normal cells [24]. Article Mattison JA, Colman RJ, Beasley TM, Allison DB, Kemnitz JW, Roth GS, Ingram DK, Weindruch R, de Cabo R, Anderson RM. Sci. Hyperosmotic stress contributes to mouse colonic inflammation through the methylation of protein phosphatase 2a. 2013;73(5):44954. Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism. CAS Improved metabolism and inflammation are also likely mechanisms through which CR may reduce tumor growth and enhance therapeutic response (Fig. 2015;64(5):163242. Intermittent energy restriction induces changes in breast gene expression and systemic metabolism. Linden MA, Lopez KT, Fletcher JA, Morris EM, Meers GM, Siddique S, Laughlin MH, Sowers JR, Thyfault JP, Ibdah JA, et al. Box 6079, Centre-ville Station, Montral, Qubec, Canada, Jorgelindo da Veiga Moreira&Mario Jolicur, LRI, Universit Paris-Sud, CNRS, Universit Paris-Saclay, 91405, Orsay, France, MaIAGE, INRA, Universit Paris-Saclay, 78350, Jouy-en-Josas, France, Institut Cochin, Universit Paris- Descartes, 75014, Paris, France, Nosco Pharmaceuticals, 75015, Paris, France, Assistance Publique des Hpitaux de Paris, 149 avenue Victoria, 75004, Paris, France, You can also search for this author in https://doi.org/10.1186/s12916-017-0873-x, DOI: https://doi.org/10.1186/s12916-017-0873-x. These CR mimetics affect systemic and tumor-specific inflammation and metabolism, and targeting these pathways may sensitize cancers to traditional and emerging anti-cancer therapies by reducing tumor-associated inflammation or causing metabolic stress in the cancer cell.
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