Novel role of NOX in supporting aerobic glycolysis in cancer cells with mitochondrial dysfunction and as a potential target for cancer therapy
Elevated aerobic glycolysis in cancer cells (the Warburg effect) may be attributed to respiration injury or mitochondrial dysfunction, but the underlying mechanisms and therapeutic significance remain elusive. Here we report that induction of mitochondrial respiratory defect by tetracycline-controll...
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| Published in: | PLoS biology Vol. 10; no. 5; p. e1001326 |
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| Main Authors: | , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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01-05-2012
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| Abstract | Elevated aerobic glycolysis in cancer cells (the Warburg effect) may be attributed to respiration injury or mitochondrial dysfunction, but the underlying mechanisms and therapeutic significance remain elusive. Here we report that induction of mitochondrial respiratory defect by tetracycline-controlled expression of a dominant negative form of DNA polymerase γ causes a metabolic shift from oxidative phosphorylation to glycolysis and increases ROS generation. We show that upregulation of NOX is critical to support the elevated glycolysis by providing additional NAD+. The upregulation of NOX is also consistently observed in cancer cells with compromised mitochondria due to the activation of oncogenic Ras or loss of p53, and in primary pancreatic cancer tissues. Suppression of NOX by chemical inhibition or genetic knockdown of gene expression selectively impacts cancer cells with mitochondrial dysfunction, leading to a decrease in cellular glycolysis, a loss of cell viability, and inhibition of cancer growth in vivo. Our study reveals a previously unrecognized function of NOX in cancer metabolism and suggests that NOX is a potential novel target for cancer treatment. |
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| AbstractList | Elevated aerobic glycolysis in cancer cells (the Warburg effect) may be attributed to respiration injury or mitochondrial dysfunction, but the underlying mechanisms and therapeutic significance remain elusive. Here we report that induction of mitochondrial respiratory defect by tetracycline-controlled expression of a dominant negative form of DNA polymerase γ causes a metabolic shift from oxidative phosphorylation to glycolysis and increases ROS generation. We show that upregulation of NOX is critical to support the elevated glycolysis by providing additional NAD+. The upregulation of NOX is also consistently observed in cancer cells with compromised mitochondria due to the activation of oncogenic Ras or loss of p53, and in primary pancreatic cancer tissues. Suppression of NOX by chemical inhibition or genetic knockdown of gene expression selectively impacts cancer cells with mitochondrial dysfunction, leading to a decrease in cellular glycolysis, a loss of cell viability, and inhibition of cancer growth in vivo. Our study reveals a previously unrecognized function of NOX in cancer metabolism and suggests that NOX is a potential novel target for cancer treatment. Elevated aerobic glycolysis in cancer cells (the Warburg effect) may be attributed to respiration injury or mitochondrial dysfunction, but the underlying mechanisms and therapeutic significance remain elusive. Here we report that induction of mitochondrial respiratory defect by tetracycline-controlled expression of a dominant negative form of DNA polymerase y causes a metabolic shift from oxidative phosphorylation to glycolysis and increases ROS generation. We show that upregulation of NOX is critical to support the elevated glycolysis by providing additional [NAD.sup.+]. The upregulation of NOX is also consistently observed in cancer cells with compromised mitochondria due to the activation of oncogenic Ras or loss of p53, and in primary pancreatic cancer tissues. Suppression of NOX by chemical inhibition or genetic knockdown of gene expression selectively impacts cancer cells with mitochondrial dysfunction, leading to a decrease in cellular glycolysis, a loss of cell viability, and inhibition of cancer growth in vivo. Our study reveals a previously unrecognized function of NOX in cancer metabolism and suggests that NOX is a potential novel target for cancer treatment. Elevated aerobic glycolysis in cancer cells (the Warburg effect) may be attributed to respiration injury or mitochondrial dysfunction, but the underlying mechanisms and therapeutic significance remain elusive. Here we report that induction of mitochondrial respiratory defect by tetracycline-controlled expression of a dominant negative form of DNA polymerase γ causes a metabolic shift from oxidative phosphorylation to glycolysis and increases ROS generation. We show that upregulation of NOX is critical to support the elevated glycolysis by providing additional NAD+. The upregulation of NOX is also consistently observed in cancer cells with compromised mitochondria due to the activation of oncogenic Ras or loss of p53, and in primary pancreatic cancer tissues. Suppression of NOX by chemical inhibition or genetic knockdown of gene expression selectively impacts cancer cells with mitochondrial dysfunction, leading to a decrease in cellular glycolysis, a loss of cell viability, and inhibition of cancer growth in vivo. Our study reveals a previously unrecognized function of NOX in cancer metabolism and suggests that NOX is a potential novel target for cancer treatment. NAD(P)H oxidase plays a role in cancer metabolism by providing NAD + to support increased glycolysis. Elevated aerobic glycolysis in cancer cells (the Warburg effect) may be attributed to respiration injury or mitochondrial dysfunction, but the underlying mechanisms and therapeutic significance remain elusive. Here we report that induction of mitochondrial respiratory defect by tetracycline-controlled expression of a dominant negative form of DNA polymerase γ causes a metabolic shift from oxidative phosphorylation to glycolysis and increases ROS generation. We show that upregulation of NOX is critical to support the elevated glycolysis by providing additional NAD+. The upregulation of NOX is also consistently observed in cancer cells with compromised mitochondria due to the activation of oncogenic Ras or loss of p53, and in primary pancreatic cancer tissues. Suppression of NOX by chemical inhibition or genetic knockdown of gene expression selectively impacts cancer cells with mitochondrial dysfunction, leading to a decrease in cellular glycolysis, a loss of cell viability, and inhibition of cancer growth in vivo. Our study reveals a previously unrecognized function of NOX in cancer metabolism and suggests that NOX is a potential novel target for cancer treatment. Glycolysis is a cytoplasmic metabolic process that produces energy from glucose. In normal cells, the rate of glycolysis is low, and glycolysis products are further processed in the mitochondria via oxidative phosphorylation, a very efficient energy-producing process. Cancer cells, however, display higher levels of glycolysis followed by cytoplasmic fermentation, and reduced levels of oxidative phosphorylation. It was thought that increased glycolysis is associated with mitochondrial dysfunction, but how these phenomena are functionally linked was not known. Understanding how these processes are regulated will be essential for developing more effective anti-cancer therapies. Here, we show that induction of mitochondrial dysfunction by either genetic or chemical approaches results in a switch from oxidative phosphorylation to glycolysis. We further show that NADPH oxidase (NOX), an enzyme known to catalyze the oxidation of NAD(P)H, also plays a critical role in supporting increased glycolysis in cancer cells by generating NAD + , a substrate for one of the key glycolytic reactions. Inhibition of NOX leads to inhibition of cancer cell proliferation in vitro and suppression of tumor growth in vivo. This study reveals a novel function for NOX in cancer metabolism, explains the increased glycolysis observed in cancer cells, and identifies NOX as a potential anti-cancer therapeutic target. |
| Audience | Academic |
| Author | Zhang, Hui Wang, Huamin Luo, Yongde Hu, Yumin McKeehan, Wallace Keating, Michael J Wang, Feng Chen, Zhao Feng, Li Chen, Gang Pelicano, Helene Liu, Jinsong Lu, Weiqin Wang, Hua Huang, Peng |
| AuthorAffiliation | 2 State Key Laboratory of Oncology in Southern China, Sun Yat-Sen University Cancer Center, Guangzhou, China 3 Department of GI Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America 6 Proteomics and Nanotechnology Laboratory, Center for Cancer and Stem Cell Biology, Institute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, Texas, United States of America University of Wuerzburg, Germany 4 Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America 5 Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America 1 Department of Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America |
| AuthorAffiliation_xml | – name: 2 State Key Laboratory of Oncology in Southern China, Sun Yat-Sen University Cancer Center, Guangzhou, China – name: 6 Proteomics and Nanotechnology Laboratory, Center for Cancer and Stem Cell Biology, Institute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, Texas, United States of America – name: 1 Department of Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America – name: 5 Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America – name: University of Wuerzburg, Germany – name: 3 Department of GI Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America – name: 4 Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America |
| Author_xml | – sequence: 1 givenname: Weiqin surname: Lu fullname: Lu, Weiqin organization: Department of Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America – sequence: 2 givenname: Yumin surname: Hu fullname: Hu, Yumin – sequence: 3 givenname: Gang surname: Chen fullname: Chen, Gang – sequence: 4 givenname: Zhao surname: Chen fullname: Chen, Zhao – sequence: 5 givenname: Hui surname: Zhang fullname: Zhang, Hui – sequence: 6 givenname: Feng surname: Wang fullname: Wang, Feng – sequence: 7 givenname: Li surname: Feng fullname: Feng, Li – sequence: 8 givenname: Helene surname: Pelicano fullname: Pelicano, Helene – sequence: 9 givenname: Hua surname: Wang fullname: Wang, Hua – sequence: 10 givenname: Michael J surname: Keating fullname: Keating, Michael J – sequence: 11 givenname: Jinsong surname: Liu fullname: Liu, Jinsong – sequence: 12 givenname: Wallace surname: McKeehan fullname: McKeehan, Wallace – sequence: 13 givenname: Huamin surname: Wang fullname: Wang, Huamin – sequence: 14 givenname: Yongde surname: Luo fullname: Luo, Yongde – sequence: 15 givenname: Peng surname: Huang fullname: Huang, Peng |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22589701$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | COPYRIGHT 2012 Public Library of Science 2012 Lu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Lu W, Hu Y, Chen G, Chen Z, Zhang H, et al. (2012) Novel Role of NOX in Supporting Aerobic Glycolysis in Cancer Cells with Mitochondrial Dysfunction and as a Potential Target for Cancer Therapy. PLoS Biol 10(5): e1001326. doi:10.1371/journal.pbio.1001326 Lu et al. 2012 |
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| Keywords | Reactive Oxygen Species Cell Survival Genes, Neoplasm Humans Oxidative Phosphorylation Gene Knockdown Techniques Tetracycline Xenograft Model Antitumor Assays Mitochondria Animals Transfection Mice, Nude Plasmids HEK293 Cells Glycolysis Mice RNA, Small Interfering Enzyme Activation Pancreatic Neoplasms NADPH Oxidase Superoxide Dismutase |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 The author(s) have made the following declarations about their contributions: Conceived and designed the experiments: WL PH . Performed the experiments: WL YH GC ZC HZ FW LF HP HW HW YL. Analyzed the data: WL YH GC HW HW YL. Contributed reagents/materials/analysis tools: WL JL MK WM YL. Wrote the paper: HP WL YH. |
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| Title | Novel role of NOX in supporting aerobic glycolysis in cancer cells with mitochondrial dysfunction and as a potential target for cancer therapy |
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