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Journal articles on the topic 'BPGM, cancer cells metabolism, Warburg effect, Reverse Warburg effect'

Author: Grafiati

Published: 14 March 2023

Last updated: 31 July 2025

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1

Gonzalez, Claudio D., Silvia Alvarez, Alejandro Ropolo, Carla Rosenzvit, Maria F. Gonzalez Bagnes, and Maria I. Vaccaro. "Autophagy, Warburg, and Warburg Reverse Effects in Human Cancer." BioMed Research International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/926729.

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Autophagy is a highly regulated-cell pathway for degrading long-lived proteins as well as for clearing cytoplasmic organelles. Autophagy is a key contributor to cellular homeostasis and metabolism. Warburg hypothesized that cancer growth is frequently associated with a deviation of a set of energy generation mechanisms to a nonoxidative breakdown of glucose. This cellular phenomenon seems to rely on a respiratory impairment, linked to mitochondrial dysfunction. This mitochondrial dysfunction results in a switch to anaerobic glycolysis. It has been recently suggested that epithelial cancer cell

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Pokorný, Jiří, Jan Pokorný, Jitka Kobilková, Anna Jandová, Jan Vrba, and Jan Vrba. "Targeting Mitochondria for Cancer Treatment – Two Types of Mitochondrial Dysfunction." Prague Medical Report 115, no. 3-4 (2014): 104–19. http://dx.doi.org/10.14712/23362936.2014.41.

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Two basic types of cancers were identified – those with the mitochondrial dysfunction in cancer cells (the Warburg effect) or in fibroblasts supplying energy rich metabolites to a cancer cell with functional mitochondria (the reverse Warburg effect). Inner membrane potential of the functional and dysfunctional mitochondria measured by fluorescent dyes (e.g. by Rhodamine 123) displays low and high values (apparent potential), respectively, which is in contrast to the level of oxidative metabolism. Mitochondrial dysfunction (full function) results in reduced (high) oxidative metabolism, low (hig

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Schiliro, Chelsea, and Bonnie L. Firestein. "Mechanisms of Metabolic Reprogramming in Cancer Cells Supporting Enhanced Growth and Proliferation." Cells 10, no. 5 (2021): 1056. http://dx.doi.org/10.3390/cells10051056.

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Cancer cells alter metabolic processes to sustain their characteristic uncontrolled growth and proliferation. These metabolic alterations include (1) a shift from oxidative phosphorylation to aerobic glycolysis to support the increased need for ATP, (2) increased glutaminolysis for NADPH regeneration, (3) altered flux through the pentose phosphate pathway and the tricarboxylic acid cycle for macromolecule generation, (4) increased lipid uptake, lipogenesis, and cholesterol synthesis, (5) upregulation of one-carbon metabolism for the production of ATP, NADH/NADPH, nucleotides, and glutathione,

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Keller, Florian, Roman Bruch, Richard Schneider, Julia Meier-Hubberten, Mathias Hafner, and Rüdiger Rudolf. "A Scaffold-Free 3-D Co-Culture Mimics the Major Features of the Reverse Warburg Effect In Vitro." Cells 9, no. 8 (2020): 1900. http://dx.doi.org/10.3390/cells9081900.

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Most tumors consume large amounts of glucose. Concepts to explain the mechanisms that mediate the achievement of this metabolic need have proposed a switch of the tumor mass to aerobic glycolysis. Depending on whether primarily tumor or stroma cells undergo such a commutation, the terms ‘Warburg effect’ or ‘reverse Warburg effect’ were coined to describe the underlying biological phenomena. However, current in vitro systems relying on 2-D culture, single cell-type spheroids, or basal-membrane extract (BME/Matrigel)-containing 3-D structures do not thoroughly reflect these processes. Here, we a

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Parkinson, E. Kenneth, Jerzy Adamski, Grit Zahn, et al. "Extracellular citrate and metabolic adaptations of cancer cells." Cancer and Metastasis Reviews 40, no. 4 (2021): 1073–91. http://dx.doi.org/10.1007/s10555-021-10007-1.

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Abstract It is well established that cancer cells acquire energy via the Warburg effect and oxidative phosphorylation. Citrate is considered to play a crucial role in cancer metabolism by virtue of its production in the reverse Krebs cycle from glutamine. Here, we review the evidence that extracellular citrate is one of the key metabolites of the metabolic pathways present in cancer cells. We review the different mechanisms by which pathways involved in keeping redox balance respond to the need of intracellular citrate synthesis under different extracellular metabolic conditions. In this conte

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Qin, Feilu, Keying Lan, and Yue Sun. "The Role of Cancer⁃Associated Fibroblasts (Cafs) In Tumor Development." Highlights in Science, Engineering and Technology 123 (December 24, 2024): 235–42. https://doi.org/10.54097/zmw1bv40.

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Today, cancer is still the key threaten to life, and CAFs are one of the mostly studied risk factor. This article reviews the mechanism of respiration of CAFS cells in cancer like Reverse Warburg Effect of CAFs, as well as the mechanism of TGF-β/Smad, the related diseases and corresponding drugs by targeting CAFs production. In tumor microenvironment(TME), CAFs are closely associated with the development, transfer and aggression of tumor cells. ‘Reverse Warburg Effect is one of the ways for CAFs to achieve metabolic cross-talk with tumor cells. Through oxidative glycolysis, CAFs can produce pl

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Evans, Laura A., Emilie I. Anderson, Xuan-Mai Petterson, Shaji Kumar, and Wilson I. Gonsalves. "Disrupting the Reverse Warburg Effect As a Therapeutic Strategy in Multiple Myeloma." Blood 138, Supplement 1 (2021): 2649. http://dx.doi.org/10.1182/blood-2021-147970.

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Abstract Introduction: Altered cellular metabolism is a hallmark of every cancer cell. Aerobic glycolysis ("The Warburg Effect") is one of the earliest recognized metabolic abnormalities in cancer cells whereby extracellular glucose is preferentially metabolized and eventually processed to generate lactate and energy in the form of ATP before the former is released extracellularly, irrespective of oxygen availability. While extracellular lactate produced and released from cancer cells has traditionally been considered a waste metabolic by-product, recent understanding of cell metabolism sugges

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Duda, Przemysław, Jakub Janczara, James A. McCubrey, Agnieszka Gizak та Dariusz Rakus. "The Reverse Warburg Effect Is Associated with Fbp2-Dependent Hif1α Regulation in Cancer Cells Stimulated by Fibroblasts". Cells 9, № 1 (2020): 205. http://dx.doi.org/10.3390/cells9010205.

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Fibroblasts are important contributors to cancer development. They create a tumor microenvironment and modulate our metabolism and treatment resistance. In the present paper, we demonstrate that healthy fibroblasts induce metabolic coupling with non-small cell lung cancer cells by down-regulating the expression of glycolytic enzymes in cancer cells and increasing the fibroblasts’ ability to release lactate and thus support cancer cells with energy-rich glucose-derived metabolites, such as lactate and pyruvate—a process known as the reverse Warburg effect. We demonstrate that these changes resu

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Reiter, Russel J., Ramaswamy Sharma, Qiang Ma, Sergio Rosales-Corral, Dario Acuna-Castroviejo, and Germaine Escames. "Inhibition of mitochondrial pyruvate dehydrogenase kinase: a proposed mechanism by which melatonin causes cancer cells to overcome cytosolic glycolysis, reduce tumor biomass and reverse insensitivity to chemotherapy." Melatonin Research 2, no. 3 (2019): 105–19. http://dx.doi.org/10.32794/mr11250033.

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This review presents a hypothesis to explain the role of melatonin in regulating glucose metabolism in cancer cells. Many cancer cells use cytosolic glycolysis (the Warburg effect) to produce energy (ATP). Under these conditions, glucose is primarily converted to lactate which is released into the blood in large quantities. The Warburg effect gives cancer cells advantages in terms of enhanced macromolecule synthesis required for accelerated cellular proliferation, reduced cellular apoptosis which enhances tumor biomass and a greater likelihood of metastasis. Based on available data, high circu

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Li, Na, and Xianquan Zhan. "Multiomics-based energy metabolism heterogeneity and its regulation by antiparasite drug ivermectin." Journal of Clinical Oncology 38, no. 15_suppl (2020): e18080-e18080. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e18080.

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e18080 Background: Energy metabolism heterogeneity is a hallmark in ovarian cancer, namely the Warburg effect and the reverse Warburg effects coexist in ovarian cancer. Exploration of energy metabolism heterogeneity benefits for discovery of the effective biomarkers for ovarian cancers. Methods: Comprehensive analysis of mitochondrial proteomics data (1198 mitochondrial differentially expressed proteins), mitochondrial phosphorpoteomics data (67 mitochondrial phosphorproteins), proteomics data (205 differentially expressed proteins), and transcriptomics data (20115 genes in 419 ovarian cancer

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Ordway, Bryce, Michal Tomaszewski, Samantha Byrne, et al. "Targeting of Evolutionarily Acquired Cancer Cell Phenotype by Exploiting pHi-Metabolic Vulnerabilities." Cancers 13, no. 1 (2020): 64. http://dx.doi.org/10.3390/cancers13010064.

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Evolutionary dynamics can be used to control cancers when a cure is not clinically considered to be achievable. Understanding Darwinian intratumoral interactions of microenvironmental selection forces can be used to steer tumor progression towards a less invasive trajectory. Here, we approach intratumoral heterogeneity and evolution as a dynamic interaction among subpopulations through the application of small, but selective biological forces such as intracellular pH (pHi) and/or extracellular pH (pHe) vulnerabilities. Increased glycolysis is a prominent phenotype of cancer cells under hypoxia

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Peng, Bo, Si-Yuan Zhang, Ka Iong Chan, Zhang-Feng Zhong, and Yi-Tao Wang. "Novel Anti-Cancer Products Targeting AMPK: Natural Herbal Medicine against Breast Cancer." Molecules 28, no. 2 (2023): 740. http://dx.doi.org/10.3390/molecules28020740.

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Breast cancer is a common cancer in women worldwide. The existing clinical treatment strategies have been able to limit the progression of breast cancer and cancer metastasis, but abnormal metabolism, immunosuppression, and multidrug resistance involving multiple regulators remain the major challenges for the treatment of breast cancer. Adenosine 5′-monophosphate (AMP)-Activated Protein Kinase (AMPK) can regulate metabolic reprogramming and reverse the “Warburg effect” via multiple metabolic signaling pathways in breast cancer. Previous studies suggest that the activation of AMPK suppresses th

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Cai, Shasha, Qingqing Xia, Darong Duan, et al. "Creatine kinase mitochondrial 2 promotes the growth and progression of colorectal cancer via enhancing Warburg effect through lactate dehydrogenase B." PeerJ 12 (June 28, 2024): e17672. http://dx.doi.org/10.7717/peerj.17672.

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Background Mitochondrial creatine kinase (MtCK) plays a pivotal role in cellular energy metabolism, exhibiting enhanced expression in various tumors, including colorectal cancer (CRC). Creatine kinase mitochondrial 2 (CKMT2) is a subtype of MtCK; however, its clinical significance, biological functions, and underlying molecular mechanisms in CRC remain elusive. Methods We employed immunohistochemical staining to discern the expression of CKMT2 in CRC and adjacent nontumor tissues of patients. The correlation between CKMT2 levels and clinical pathological factors was assessed. Additionally, we

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Abbruzzese, Claudia, Silvia Matteoni, Paola Matarrese, et al. "Abstract 4713: Chlorpromazine affects glioblastoma bioenergetics by interfering with pyruvate kinase M2: A route for drug repurposing in glioblastoma." Cancer Research 84, no. 6_Supplement (2024): 4713. http://dx.doi.org/10.1158/1538-7445.am2024-4713.

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Abstract Glioblastoma, the most common and deadly brain tumor, remains a critical unmet medical need due to the limited effectiveness of current treatments. Drug repurposing has recently emerged as a promising strategy to improve glioblastoma outcomes. Antipsychotic drugs, with their established safety profile and potential to disrupt tumor-neuron interactions, have drawn particular attention. Among these, chlorpromazine, a well-tolerated medication included in the 2021 WHO Model List of Essential Medicines, holds promise due to its therapeutic effects in psychiatric disorders stemming from it

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Pfeilstocker, Michael, Peter Wihlidal, Franz Varga, Elisabeth Pittermann, and Heidrun Karlic. "Imatinib Mesylate Induced Reversal of Leukemic Gene Phenotype in HL60 Cells Coincides with Stimulation of Oxidative Metabolism." Blood 110, no. 11 (2007): 4190. http://dx.doi.org/10.1182/blood.v110.11.4190.4190.

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Abstract Besides blockade of tyrosine kinases such as c-kit, Imatinib mesylate (IM) regulates glucose flux through downregulation of GLUT-1 transporters in human leukemia cells. This mechanism has the potential to induce regression of type 2 diabetes and hyperlipidemia as observed in patients with chronic myeloid leukemia or hypereosinophilic syndrome. In addition, there is a stimulatory effect of IM on differentiation of human mesenchymal stem cells. Its synergism with retinoic acid or low dose Ara-C is applied in treatment of acute myeloid leukemia (AML). Thus, the AML-derived c-kit positive

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Johnson, Suzanne M., Clare Dempsey, Amy Chadwick, et al. "Metabolic Reprogramming of Bone Marrow Stromal Cells By Leukemic Extracellular Vesicles in Acute Lymphoblastic Leukemia (ALL)." Blood 126, no. 23 (2015): 1430. http://dx.doi.org/10.1182/blood.v126.23.1430.1430.

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Abstract In ALL, leukemic cells have been shown to modulate the bone marrow microenvironment through aberrant cytokine production favoring leukemic cell survival. Extracellular vesicles have also been recognised as key mediators of non-paracrine cellular interactions in cancer. This mechanism of tumor-stromal interaction has been described in chronic lymphocytic leukemia where recipient stromal cells undergo phenotypic changes. We now report a similar phenomenon in ALL. Light microscopy showed that primary ALL blasts and cell lines, released anucleate extracellular vesicles into extracellular

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17

Abukwaik, Roba, Elias Vera-Siguenza, Daniel Tennant, and Fabian Spill. "p53 Orchestrates Cancer Metabolism: Unveiling Strategies to Reverse the Warburg Effect." Bulletin of Mathematical Biology 86, no. 10 (2024). http://dx.doi.org/10.1007/s11538-024-01346-5.

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AbstractCancer cells exhibit significant alterations in their metabolism, characterised by a reduction in oxidative phosphorylation (OXPHOS) and an increased reliance on glycolysis, even in the presence of oxygen. This metabolic shift, known as the Warburg effect, is pivotal in fuelling cancer’s uncontrolled growth, invasion, and therapeutic resistance. While dysregulation of many genes contributes to this metabolic shift, the tumour suppressor gene p53 emerges as a master player. Yet, the molecular mechanisms remain elusive. This study introduces a comprehensive mathematical model, integratin

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Ji, Lijiang, Weixing Shen, Feng Zhang та ін. "Worenine reverses the Warburg effect and inhibits colon cancer cell growth by negatively regulating HIF-1α". Cellular & Molecular Biology Letters 26, № 1 (2021). http://dx.doi.org/10.1186/s11658-021-00263-y.

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Abstract Background Some natural compounds inhibit cancer cell growth in various cancer cell lines with fewer side effects than traditional chemotherapy. Here, we explore the pharmacological effects and mechanisms of worenine (isolated from Coptis chinensis) against colorectal cancer. Methods The effects of worenine on colorectal cancer cell proliferation, colony formation and cell cycle distribution were measured. Glycolysis was investigated by examining glucose uptake and consumption, lactate production, and the activities and expressions of glycolysis enzymes (PFK-L, HK2 and PKM2). HIF-1α w

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Iacobini, Carla, Martina Vitale, Giuseppe Pugliese, and Stefano Menini. "The “sweet” path to cancer: focus on cellular glucose metabolism." Frontiers in Oncology 13 (May 25, 2023). http://dx.doi.org/10.3389/fonc.2023.1202093.

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The hypoxia-inducible factor-1α (HIF-1α), a key player in the adaptive regulation of energy metabolism, and the M2 isoform of the glycolytic enzyme pyruvate kinase (PKM2), a critical regulator of glucose consumption, are the main drivers of the metabolic rewiring in cancer cells. The use of glycolysis rather than oxidative phosphorylation, even in the presence of oxygen (i.e., Warburg effect or aerobic glycolysis), is a major metabolic hallmark of cancer. Aerobic glycolysis is also important for the immune system, which is involved in both metabolic disorders development and tumorigenesis. Mor

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Shin, Eunah, and Ja Seung Koo. "Glucose Metabolism and Glucose Transporters in Breast Cancer." Frontiers in Cell and Developmental Biology 9 (September 6, 2021). http://dx.doi.org/10.3389/fcell.2021.728759.

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Breast cancer is the most common malignancy in women worldwide and is associated with high mortality rates despite the continuously advancing treatment strategies. Glucose is essential for cancer cell metabolism owing to the Warburg effect. During the process of glucose metabolism, various glycolytic metabolites, such as serine and glycine metabolites, are produced and other metabolic pathways, such as the pentose phosphate pathway (PPP), are associated with the process. Glucose is transported into the cell by glucose transporters, such as GLUT. Breast cancer shows high expressions of glucose

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Ramzy, Asmaa, Sara ElSafy, Hisham A. Elshoky, et al. "Drugless nanoparticles tune-up an array of intertwined pathways contributing to immune checkpoint signaling and metabolic reprogramming in triple-negative breast cancer." Biomedical Materials, December 2, 2022. http://dx.doi.org/10.1088/1748-605x/aca85d.

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Abstract Background and Purpose Metabolic reprogramming “Warburg effect” and immune checkpoint signaling are immunosuppressive hallmarks of Triple-Negative Breast Cancer (TNBC) contributing to the limited clinical applicability of immunotherapy. Biomaterials arise as novel tools for immunomodulation of the tumor microenvironment (TME) that can be used alongside conventional immunotherapeutics. Chitosan and lecithin are examples of versatile biomaterials with interesting immunomodulatory properties. In this study, we aimed at investigation of the role of carefully designed hybrid nanoparticles

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Wu, Fanglong, Shimeng Wang, Qingxiang Zeng та ін. "TGF-βRII regulates glucose metabolism in oral cancer-associated fibroblasts via promoting PKM2 nuclear translocation". Cell Death Discovery 8, № 1 (2022). http://dx.doi.org/10.1038/s41420-021-00804-6.

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AbstractCancer-associated fibroblasts (CAFs) are highly heterogeneous and differentiated stromal cells that promote tumor progression via remodeling of extracellular matrix, maintenance of stemness, angiogenesis, and modulation of tumor metabolism. Aerobic glycolysis is characterized by an increased uptake of glucose for conversion into lactate under sufficient oxygen conditions, and this metabolic process occurs at the site of energy exchange between CAFs and cancer cells. As a hallmark of cancer, metabolic reprogramming of CAFs is defined as reverse Warburg effect (RWE), characterized by inc

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Affinito, Alessandra, Cristina Quintavalle, Rosario Vincenzo Chianese, et al. "MCT4-driven CAF-mediated metabolic reprogramming in breast cancer microenvironment is a vulnerability targetable by miR-425-5p." Cell Death Discovery 10, no. 1 (2024). http://dx.doi.org/10.1038/s41420-024-01910-x.

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AbstractMultiple oncogenic alterations contribute to breast cancer development. Metabolic reprogramming, deeply contributing to tumor microenvironment (TME) education, is now widely recognized as a hallmark of cancer. The reverse Warburg effect induces cancer-associated fibroblasts (CAFs) to produce and secrete L-lactate, enhancing malignant characteristics such as neoangiogenesis, metastatic dissemination, and treatment resistance. Monocarboxylate transporter (MCT) 4 is involved in lactate efflux from CAFs into stromal and epithelial cells. Here, we first assess the expression of miR-425-5p a

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Barbato, Alessandro, Grazia Scandura, Fabrizio Puglisi, et al. "Mitochondrial Bioenergetics at the Onset of Drug Resistance in Hematological Malignancies: An Overview." Frontiers in Oncology 10 (December 21, 2020). http://dx.doi.org/10.3389/fonc.2020.604143.

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The combined derangements in mitochondria network, function and dynamics can affect metabolism and ATP production, redox homeostasis and apoptosis triggering, contributing to cancer development in many different complex ways. In hematological malignancies, there is a strong relationship between cellular metabolism, mitochondrial bioenergetics, interconnections with supportive microenvironment and drug resistance. Lymphoma and chronic lymphocytic leukemia cells, e.g., adapt to intrinsic oxidative stress by increasing mitochondrial biogenesis. In other hematological disorders such as myeloma, on

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Wang, Yixuan, Houkun Zhou, Ying Liu, Xingyu Zhao, Shuhao Wang, and Zhenhua Lin. "miR-485-5p/NQO1 axis drives colorectal cancer progression by regulating apoptosis and aerobic glycolysis." Cancer Cell International 25, no. 1 (2025). https://doi.org/10.1186/s12935-025-03672-7.

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Abstract Background Cancer cells undergo a metabolic shift termed the Warburg effect, transitioning from oxidative phosphorylation to aerobic glycolysis and promoting rapid tumor proliferation. Quinone oxidoreductase (NQO1), a cytosolic flavoprotein, is important for reprogramming cancer cell metabolism. Therefore, NQO1’s function in aerobic glycolysis and impact on colorectal cancer (CRC) development and progression was investigated. Methods The clinical significance of NQO1 was evaluated by analyzing online databases and was substantiated in CRC specimens. NQO1’s influence on proliferation,

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Abbruzzese, Claudia, Silvia Matteoni, Paola Matarrese, et al. "Chlorpromazine affects glioblastoma bioenergetics by interfering with pyruvate kinase M2." Cell Death & Disease 14, no. 12 (2023). http://dx.doi.org/10.1038/s41419-023-06353-3.

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AbstractGlioblastoma (GBM) is the most frequent and lethal brain tumor, whose therapeutic outcome - only partially effective with current schemes - places this disease among the unmet medical needs, and effective therapeutic approaches are urgently required. In our attempts to identify repositionable drugs in glioblastoma therapy, we identified the neuroleptic drug chlorpromazine (CPZ) as a very promising compound. Here we aimed to further unveil the mode of action of this drug. We performed a supervised recognition of the signal transduction pathways potentially influenced by CPZ via Reverse-

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Hu, Yiyi, Shaojie Jian, Weihua Yang, and Zhifang Wu. "In vitro differences analysis in proliferation and drug sensitivity of tumor-associated fibroblasts from different regions of FDG metabolism to non-small-cell lung carcinoma." Physiology 38, S1 (2023). http://dx.doi.org/10.1152/physiol.2023.38.s1.5735343.

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Objective: 18F-FDG PET can directly reflect the glucose metabolism level of cells from the molecular level. Tumor-associated fibroblasts, as the natural physiological barrier of tumors, support and protect the survival of non-small cell lung cancer cells. This study will further observe the differences in the supporting effects of CAFs from different regions of 18F-FDG PET metabolism on cancer cells. Methods: Biopsy tissues were collected from PET/CT patients diagnosed with NSCLC for the first time in the Department of Nuclear Medicine, The First Hospital of Shanxi Medical University. The loca

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Sauvaget, Melanie, Sarah-eve Lemay, Sandra Breuils Bonnet, et al. "Abstract 12681: Implication of Aurora Kinase B in Pulmonary Arterial Hypertension." Circulation 144, Suppl_1 (2021). http://dx.doi.org/10.1161/circ.144.suppl_1.12681.

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Objective: Pulmonary arterial hypertension (PAH) is a vascular disease characterized by a progressive remodelling of pulmonary arteries (PAs). This leads to an elevation in PA pressure and resistance, leading to right heart failure and death. Nowadays, it is recognized that PA smooth muscle cells (PASMCs) are key actors in the histopathological changes in PAH. As seen in cancer cells, PASMCs exhibit a pro-proliferative and anti-apoptotic cancer-like phenotype, sustained by an important metabolic switch known as Warburg effect. Aurora kinase B (AURKB) is strongly involved in cell proliferation,

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