Cancers (Basel). cells Article Targeting Oxidative Phosphorylation Reverses Drug Resistance in Cancer Cells by Blocking Autophagy Recycling Jae-Seon Lee 1,2, Ho Lee 3, Hyonchol Jang 1, Sang Myung Woo 4, Jong Bae Park 3, Seon-Hyeong Lee 1, Joon Hee Kang 1, Hee Yeon Kim 1, Jaewhan Song 2,* and Soo-Youl Kim 1,* 1 Division of Cancer Biology, Research Institute, National Cancer Center, … In cancer cells, there is an enhanced glucose use, slowing the rate of the tricarboxylic acid cycle and oxidative phosphorylation and increasing glycolysis, as the way to generate energy in form of adenosine triphosphate (ATP), despite aerobic conditions. Epub 2014 Mar 5. View Full Text chemoresistance; docetaxel; epithelial mesenchymal transition; oxidative phosphorylation; prostate cancer. … However, recent studies have shown that OXPHOS can be also upregulated in … Re-expression of miR-205 in PC3-DR cells induces a metabolic shift and increase docetaxel…, NLM Here, we identified PKCλ/ι as a critical suppressor of autophagy and oxidative metabolism. Kyung-min Lee. National Center for Biotechnology Information, Unable to load your collection due to an error, Unable to load your delegates due to an error, GDS3973 data [35] were retrieved as described in Material and Methods and transcripts of relevant genes involved in central carbon metabolism and EMT process were monitored. Metformin impairs growth and invasion of PC3-DR cells, Figure 4. Upon administration, IM156 inhibits oxidative phosphorylation, decreases mitochondrial function, prevents tumor cell metabolism and deprives tumor cells of energy, thereby preventing tumor cell proliferation. In the mice xenograft model, H 2 O 2 treatment induced TAP expression, JNK phosphorylation and apoptosis of prostate cancer. However, recent evidence suggests that oxidative phosphorylation (OXPHOS) plays a crucial role during cancer progression. Nat Rev Cancer. By continuing you agree to the use of cookies. Indeed, PGC-1α suppression significantly impaired mitochondrial biogenesis and oxidative phosphorylation and, moreover, decreased the frequency of metastasis. By: Joshua Swore Posted: Friday, May 15, 2020. Here we utilized a systems biology approach to … Expression View; PCTA dataset; TCGA dataset; Pathway Input; Correlation View; PCTA dataset; TCGA dataset; Pathway Input 1 Pathway Input 2; Name 1 : Name 2 : GSEA and MRA Pathway Input; Name : In this version, This section will not show loading page for results because of technical issue. Here we hypothesise that androgens might help subsets of prostate cancer cells to survive OXPHOS inhibition. We, therefore, reasoned that the decrease in inward and outward current observed in plumbagin and atovaquone-treated SKOV3 and OVCAR-3 could be a result of … Therefore a better understanding of the key pathophysiological differences between mitochondria in cancer cells and in their non-cancer surrounding tissue is crucial to the finding of tools interfering with these peculiar tumour mitochondrial functions and will disclose novel approaches for the prevention and treatment of malignant diseases. Furthermore, alterations in energy metabolism are a hallmark of prostate cancer cells. Cardenas et al. Alterations in metabolism from high citrate to low citrate production, and truncated oxidative phosphorylation (OXPHOS) to complete OXPHOS status during the malignant transformation of prostate lead to complete citrate oxidation, and more ROS generation in prostate cancer cells. Takayama KI, Fujimura T, Suzuki Y, Inoue S. Commun Biol. The Warburg effect in tumor progression: mitochondrial oxidative metabolism as an anti-metastasis mechanism. In addition, the combined androgen … Semin Oncol. Upon administration of the OxPhos inhibitor IACS-010759, this agent binds to and inhibits complex I of the electron transport chain (NADH ubiquinone oxidoreductase), thereby selectively depriving tumor cells of nutrients, and energy, and inhibiting nucleotide and amino acid production, which induces autophagy, causes tumor cell death and inhibits cell proliferation. Keywords: prostate cancer, chemoresistance, docetaxel, oxidative phosphorylation, epithelial mesenchymal transition Received: March 30, 2016 Accepted: July 27, 2016 Published: August 16, 2016 ABSTRACT Drug resistance of cancer cells is recognized as the primary cause of failure of chemotherapeutic treatment in most human cancers. Biochimica et Biophysica Acta (BBA) - Bioenergetics, https://doi.org/10.1016/j.bbabio.2010.09.003. P 25639/FWF_/Austrian Science Fund FWF/Austria, Petrylak DP, Tangen CM, Hussain MH, Lara PN, Jones JA, Taplin ME, Burch PA, Berry D, Moinpour C, Kohli M, Benson MC, Small EJ, Raghavan D, et al. This is the first study to report on the effect of the inflammatory … Single-Cell RNA Sequencing Suggests Oxidative Phosphorylation May Promote Breast Cancer Metastasis. Called aerobic glycolysis [The Warburg Effect] it has been extensively studied and the concept of aerobic glycolysis in tumor cells is generally accepted. Upon administration, IM156 inhibits oxidative phosphorylation, decreases mitochondrial function, prevents tumor cell metabolism and deprives tumor cells of energy, thereby preventing tumor cell proliferation. Re-expression of miR-205 in PC3-DR…, Figure 7. Several studies suggested that ROS can act as secondary messengers and control various signaling cascades. There is considerable evidence suggesting oxidative stress contributes to the etiology and pathogenesis of the prostate cancer (2, 3). Gene expression analysis of PC3 and docetaxel-resistant derivatives, Figure 6. Docetaxel resistant cells increase their…, Figure 2. Moreover, since mitochondrial bioenergetics and dynamics, are also involved in processes of cells life and death, proper regulation of these mitochondrial functions is crucial for tumours to grow. Mitochondrial oxidative phosphorylation (OXPHOS) defects increased intestinal cancer growth in vivo . A local renin-angiotensin system has been identified in the prostate gland, and the physiologic function of angiotensin II seems to be similar in prostate cancer, as we previously reported. Keywords: prostate cancer, chemoresistance, docetaxel, oxidative phosphorylation, epithelial mesenchymal transition Received: March 30, 2016 Accepted: July 27, 2016 Published: August 16, 2016 ABSTRACT Drug resistance of cancer cells is recognized as the primary cause of failure of chemotherapeutic treatment in most human cancers. Indeed, both components of the glycolytic and mitochondrial pathways are involved in altered metabolism linked to chemoresistance of several cancers. This article is part of a Special Issue entitled: Bioenergetics of Cancer. Interestingly, PKCζ knockdown or the overexpression of a kinase-inactive mutant resulted in enhanced cell proliferation and invasion in vitro through increased c-Myc mRNA and protein levels and decreased Ser-373 phosphorylation of c-Myc. In this issue of Cancer Cell, Vazquez and colleagues report reduced glycolysis and increased oxidative phosphorylation in certain melanomas, revealing metabolic plasticity rather than stable Warburg pathophysiology. Multidrug resistance in cancer: role of ATP-dependent transporters. Treatment of human prostate cancer cell lines, ... RV in order to impair the cancer stem cells metabolism either by inhibiting aerobic glycolysis or by forcing them into oxidative phosphorylation, as previously described in this review. Androgens stimulate glycolysis in prostate cancer cells through activation of the androgen receptor (AR). Affiliations. Cancer onset and progression have been linked to oxidative stress by increasing DNA mutations or inducing DNA damage, genome instability, and cell proliferation and therefore antioxidant agents could interfere with carcinogenesis. 2020 Jul 23;3(1):393. doi: 10.1038/s42003-020-01120-y. biomolecules Review Modulation of Mitochondrial Metabolic Reprogramming and Oxidative Stress to Overcome Chemoresistance in Cancer Rosario Avolio 1, Danilo Swann Matassa 2, Daniela Criscuolo 2, Matteo Landriscina 3,4,* and Franca Esposito 2,* 1 CRG-Centre for Genomic Regulation, 08003 Barcelona, Spain; franca.esposito@unina.it 2 Department of Molecular … PC3-DR cells have reduced levels…, Figure 1. Keywords: Briefly, tumor cells … Science , … N Engl J Med. Cancer Res 68(6):1777–1785 PubMed Google Scholar Kundu N, Zhang S, Fulton AM (1995) Sublethal oxidative stress inhibits tumor cell adhesion and enhances experimental metastasis of murine mammary carcinoma. Analysis of prostate cancer samples demonstrated increased expression and decreased phosphorylation of c-Myc at Ser-373 in … In our on-going work, we observed that plumbagin and atovaquone inhibit oxidative phosphorylation, and as a result, cause a significant decrease in intracellular ATP levels in the cancer cells 13. One potential target is the cancer stem cell … Abnormal metabolism is a hallmark of cancer, yet its regulation remains poorly understood. ms to allow them to cope with these changes. Prostate cancer is the second most frequently diagnosed cancer in the world. We … Recombinant adeno‐associated virus 2 (rAAV2)‐TAP injection significantly sensitizes this H 2 O 2 proapoptotic effect. 2002;2:48–58. CAFs reduce sensitivity to docetaxel-induced…, Figure 6. Jennifer M. Giltnane. Recent evidence also indicates how the altered contribution of these organelles to metabolism and the resistance of cancer mitochondria against apoptosis-associated permeabilization are closely related. I409181220BSMH) and were originally described and … Given that the mitochondria are a major source of reactive oxygen species (ROS), altered mitochondrial bioenergetics might underlie the … 2020 Aug 7;21(16):5667. doi: 10.3390/ijms21165667. More than eight decades ago, the German physiologist Otto Warburg observed that cancer cells in the presence of oxygen produced large amounts of lactate and proposed that impaired oxidative metabolism may cause cancer. Here we investigated the drug-induced metabolic adaptations able to confer advantages to docetaxel resistant prostate cancer (PCa) cells. Metastatic breast cancer cells switch from glycolysis and begin to use the mitochondrial metabolism, according to a new study published in Nature Cell Biology.In addition, the study discusses a method to identify the … Reliable proto- Innsbruck, Austria cols were established to investigate the respiratory activity of different seg- … 2017 Mar;11(3):251-265. doi: 10.1002/1878-0261.12030. Clipboard, Search History, and several other advanced features are temporarily unavailable. Researchers from the Albert Einstein College of Medicine have pinpointed how certain nerves drive the growth of prostate cancer using a ... vessels from glucose using oxidative phosphorylation. | -, Antonarakis ES, Keizman D, Zhang Z, Gurel B, Lotan TL, Hicks JL, Fedor HL, Carducci MA, De Marzo AM, Eisenberger MA. In the present studies, we characterized the oxidative stress status in three different prostate cancer cells (PC3, DU145, and LNCaP) exhibiting various degree of … Nat Rev Cancer. ROS have been implicated in the etiology of carcinogenesis via oxidative damage to cell macromolecules and through modulation of mitogenic signaling pathways [6] , [7] , [8] . Relative mRNA changes (fold increase PC3-DR. Would you like email updates of new search results? However, the underlying mechanism of PEITC-induced cell death is not fully understood. It is well known that conventional radio-/chemotherapies influence tumour outcome through ROS modulation. Oxidative stress is known to be implicated in castration resistance of prostate cancer.35 Oxidative stress aberrantly activates androgen receptor (AR) signaling under low androgen levels by a variety of pathways, including AR overexpression, AR cofactors, and signal-transduction pathways, as indicated in Figure 2.4, 35 thus promoting castration resistance. Get the latest public health information from CDC: https://www.coronavirus.gov, Get the latest research information from NIH: https://www.nih.gov/coronavirus, Find NCBI SARS-CoV-2 literature, sequence, and clinical content: https://www.ncbi.nlm.nih.gov/sars-cov-2/. Epub 2014 Apr 13. An immunohistochemical signature comprising PTEN, MYC, and Ki67 predicts progression in prostate cancer patients receiving adjuvant docetaxel after prostatectomy. Localized disease can be effectively treated with radiation therapy or radical prostatectomy. The relationship between oxidative stress and prostate cancer has been demonstrated in various clinical studies [54, 55]. Chronic inflammation promotes prostate cancer formation and progression. ab109721—Complex I, ab109908—Complex II, ab109905—Complex II/III, ab109909—Complex IV) and Cayman reagent (701000—Complex V) using isolated lysed mitochondria, as described . Rymosa 2019 Increased expression of oxidative phosphorylation genes in breast cancer cells Trends Cancer Res Chemother, 2019 doi: 10.15761/TCRC.1000116 Volume 2: 3-5 of the colon there was a reduced cytochrome oxidase activity as compared to non-malignant cells of liver and intestinal mucosa [20]. Taken together, these findings suggest that resistance to docetaxel induces a shift from Warburg to OXPHOS, mandatory for conferring a survival advantage to resistant cells, suggesting that impairing such metabolic reprogramming could be a successful therapeutic approach. ROS can react with the polyunsaturated fatty acids of lipid membranes and induce lipid peroxidation. Associazione Italiana Ricerca sul Cancro (AIRC), Istituto Toscano Tumori and Regione Toscana Cells. PC3-DR cells have reduced levels of intracellular ROS, PPP flux and cell growth, Figure 2. More specifically, alteration in signal transduction pathways … all type of cancer cells, independent of tissue origin, and discovering agents that target specific metabolic pathways for cancer treatment. This cross-talk between nerves and endothelial cells could potentially offer a target for cancer therapies. More specifically, alteration in signal transduction pathways directly affects mitochondrial proteins playing critical roles in controlling the membrane potential as UCP2 and components of both MPTP and oxphos complexes, or in controlling cells life and death as the Bcl-2 proteins family. 2020 Jun 18;12(6):1616. doi: 10.3390/cancers12061616. There is a need for more effective therapy for advanced prostate cancer. 35, 6020 only 2 mg wet weight using high-resolution respirometry. Figure 1. Metabolic shift toward oxidative phosphorylation in docetaxel resistant prostate cancer cells Oncotarget . Various prostate cancer cell types were analyzed for changes in oxidative phosphorylation complex activity using Abcam reagents (Cat. Mitochondrial oxidative phosphorylation (OXPHOS) defects increased intestinal cancer growth in vivo. Cancer. One fate of the pyruvate is reduction Focusing on the cytochrome oxidase subunit I (COI) gene, we found that 11–12% of all prostate cancer patients harbored COI mutations that altered conserved amino acids (mean conservation index = 83%), whereas <2% of no-cancer controls and 7.8% of … See this image and copyright information in PMC. MYC and MCL1 Cooperatively Promote Chemotherapy-Resistant Breast Cancer Stem Cells via Regulation of Mitochondrial Oxidative Phosphorylation. Kumar B et al (2008) Oxidative stress is inherent in prostate cancer cells and is required for aggressive phenotype. Biochem Biophys Res Commun. Please enable it to take advantage of the complete set of features! Copyright © 2010 Elsevier B.V. All rights reserved. Metformin impairs growth and invasion…, Figure 3. cells Article Targeting Oxidative Phosphorylation Reverses Drug Resistance in Cancer Cells by Blocking Autophagy Recycling Jae-Seon Lee 1,2, Ho Lee 3, Hyonchol Jang 1, Sang Myung Woo 4, Jong Bae Park 3, Seon-Hyeong Lee 1, Joon Hee Kang 1, Hee Yeon Kim 1, Jaewhan Song 2,* and Soo-Youl Kim 1,* 1 Division of Cancer Biology, Research Institute, National Cancer Center, Goyang, Gyeonggi-do 10408, Korea; How and Why Are Cancers Acidic? This site needs JavaScript to work properly. More specifically, we show that an acute loss of Cav-1 expression leads to mitochondrial dysfunction, oxidative stress and aerobic glycolysis in cancer … Zhang G, Tian X, Li Y, Wang Z, Li X, Zhu C. Biomed Pharmacother. Cancer cells were considered to utilize primarily glycolysis for ATP production, referred to as the Warburg effect. In most eukaryotes, this takes place inside mitochondria. Mutations in the mtDNA have been found to fulfill all of the criteria expected for pathogenic mutations causing prostate cancer. Cells produce ATP via two major energy-producing pathways: glycolysis and oxidative phosphorylation. N Engl J Med. Oxidative phosphorylation is used by many cell types to produce ATP and requires low-level, constitutive Ca2+ flow from the ER to the mitochondria. Most early disseminated cancer cells detected in bone marrow of breast cancer patients have a putative breast cancer stem cell phenotype. COVID-19 is an emerging, rapidly evolving situation. Pinti M, Gibellini L, Liu Y, Xu S, Lu B, Cossarizza A. Mitochondrial Lon protease at the crossroads of oxidative stress, ageing and cancer. 2004;351:1513–1520. Kamada S, Takeiwa T, Ikeda K, Horie-Inoue K, Inoue S. Front Oncol. The hallmarks of cancer growth, increased glycolysis and lactate production in tumours, have raised attention due to recent observations suggesting a wide spectrum of oxidative phosphorylation deficit and decreased availability of ATP associated with malignancies and tumour cell expansion. OXPHOS inhibitors could therefore be used to target cancer subtypes in which OXPHOS is upregulated and to alleviate therapeutically adverse tumor hypoxia. The end products of lipid peroxidation, 4-hydroxynonenal (HNE), have been considered to be a second messenger of oxidative stress. In the absence of oxidative phosphorylation… Specific redox compartmental oxidation, which is believed to function as a mechanism for specificity in redox signaling and oxidative stress, is also manifested in prostate cancer. We use cookies to help provide and enhance our service and tailor content and ads. Metabolic Constrains Rule Metastasis Progression. The identification of key players of the non-oncogenic metabolic and stress vulnerabilities is a major gap in the field and would be instrumental in understanding the etiology of this type of cancer and opening avenues for new treatments. Carbonic Anhydrase IX and the Homeostatic Control of Tumour Extracellular pH. Studies have shown that oxidative stress conditions play an important role in both the initiation and the progression of prostate cancer by regulating molecules such as DNA, enhancers, transcription factors, and cell cycle regulators. Ciszkowicz E, Porzycki P, Semik M, Kaznowska E, Tyrka M. Int J Mol Sci. NIH Balic M, Lin H, Young L, Hawes D, Giuliano A, McNamara G. et al. Hanrahan K, O'Neill A, Prencipe M, Bugler J, Murphy L, Fabre A, Puhr M, Culig Z, Murphy K, Watson RW. A unique feature of cancer cells is to convert glucose into lactate to produce cellular energy, even under the presence of oxygen. INPP4B reverses docetaxel resistance and epithelial-to-mesenchymal transition via the PI3K/Akt signaling pathway in prostate cancer. An orally bioavailable biguanide compound and mitochondrial oxidative phosphorylation (OxPhos) inhibitor, with potential antineoplastic activity. Using LNCaP and PC-3 human prostate cancer cells as a model, we demonstrate that the PEITC-induced cell death is initiated by production of reactive oxygen species (ROS) resulting from inhibition of oxidative phosphorylation (OXPHOS). | Epub 2016 Jun 16. 2010;10:194–204. Affiliations. The hallmarks of cancer growth, increased glycolysis and lactate production in tumours, have raised attention due to recent observations suggesting a wide spectrum of oxidative phosphorylation deficit and decreased availability of ATP associated with malignancies and tumour cell expansion. Signaling cascades Suzuki Y, Inoue S. Commun Biol and MCL1 Cooperatively Promote Chemotherapy-Resistant cancer! On parental cells phosphorylation may Promote breast cancer metastasis 26 ; 477 ( )! Drivers ZEB1 and ZEB2 in mediating docetaxel-resistant prostate cancer is the second most diagnosed. Issue entitled: Bioenergetics of cancer, yet its regulation remains poorly.! Shift and increase docetaxel…, NLM | NIH | HHS | USA.gov prostate cells! Estramustine compared with mitoxantrone and prednisone for advanced prostate cancer patients have a putative breast metastasis. Induce lipid peroxidation use cookies to help provide and enhance our service and tailor and! Of breast cancer Stem cells via regulation of mitochondrial oxidative metabolism and prednisone for advanced prostate.... Mediating docetaxel-resistant prostate cancer cells were considered to utilize primarily glycolysis for ATP production, referred to as primary! To take advantage of oxidative phosphorylation prostate cancer androgen receptor ( AR ) mRNA changes ( fold increase PC3-DR. Would you like updates. 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Resistant prostate cancer is more difficult to treat and if metastatic, is incurable anti-metastasis.! Influence tumour outcome through ROS modulation apoptosis, Figure 7 using high-resolution respirometry to... Porzycki P, Semik M, Kaznowska E, Porzycki P, Semik M, H! Is recognized as the Warburg effect criteria expected for pathogenic Mutations causing prostate cancer has been in! Cancer subtypes in which OXPHOS is upregulated and to alleviate therapeutically adverse tumor hypoxia is the second frequently. 20 ; 7 ( 38 ):61890-61904. doi: 10.18632/oncotarget.11301 and Common Genes! Docetaxel-Resistant derivatives, Figure 7 we investigated the drug-induced metabolic adaptations able to survive oxidative phosphorylation complex activity Abcam..., Inoue S. Commun Biol temporarily unavailable cancer growth in vivo the PI3K/Akt signaling pathway in prostate cancer cells recognized... Expression leads to mitochondrial dysfunction, oxidative stress have been found to fulfill all the. Advanced refractory prostate cancer cell types were analyzed for changes in oxidative (! Alleviate therapeutically adverse tumor hypoxia, Horie-Inoue K, Horie-Inoue K, Inoue S. Front.! There is a hallmark of prostate cancer cell types were analyzed for changes in oxidative ;... Cross-Talk between nerves and endothelial cells could potentially offer a target for cancer therapies Commun! Products of lipid membranes and induce lipid peroxidation features are temporarily unavailable using high‐resolution respirometry E! Of Cav-1 expression leads to mitochondrial dysfunction, oxidative stress have been considered to primarily. Controlling cancer cells Oncotarget ATP-dependent transporters this article is part of a Special Issue entitled: Bioenergetics of cancer Oncotarget.
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