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Molecular Cancer (2024) 23:203 [https://doi.org/10.1186/s12943-024-02119-3](https://doi.org/10.1186/s12943-024-02119-3)  \nMolecular Cancer  \n REVIEW Open Access  \nAltered metabolism in cancer: insights  \ninto energy pathways and therapeutic targets  \nMuhammad Tufail1 , Can-Hua Jiang1,2,3,4 and Ning Li 1,2,3,4*  \nAbstract  \nCancer cells undergo significant metabolic reprogramming to support their rapid growth and survival. This study examines important metabolic pathways like glycolysis, oxidative phosphorylation, glutaminolysis, and lipid metabolism, focusing on how they are regulated and their contributions to the development of tumors. The interplay between oncogenes, tumor suppressors, epigenetic modifications, and the tumor microenvironment in modulating these pathways is examined. Furthermore, we discuss the therapeutic potential of targeting cancer metabolism, presenting inhibitors of glycolysis, glutaminolysis, theTCA cycle, fatty acid oxidation, LDH, and glucose transport, alongside emerging strategies targeting oxidative phosphorylation and lipid synthesis. Despite the promise, challenges such as metabolic plasticity and the need for combination therapies and robust biomarkers persist, underscoring the necessity for continued research in this dynamic field.  \nKeywords Cancer metabolism, Glycolysis, Oxidative phosphorylation, Glutaminolysis, Lipid metabolism  \n*Correspondence: Ning Li[liningoms@csu.edu.cn](liningoms@csu.edu.cn)  \nFull list of author information is available at the end of the article  \n© The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://creativecommons.org/licenses/by-nc-nd/4.0/](http://creativecommons.org/licenses/by-nc-nd/4.0/.)[.](http://creativecommons.org/licenses/by-nc-nd/4.0/.)  \nTufail etal. Molecular Cancer (2024) 23:203 Page 2 of 40  \nGraphical Abstract  \nIntroduction  \nCancer remains one of the leading causes of morbidity and mortality worldwide. Despite significant advancements in our understanding and treatment of cancer, the complexity and adaptability of malignant cells continue to pose ongoing challenges [1, 2]. One of the hallmark features of cancer cells is their altered metabolism, which supports rapid growth and survival in hostile environments [3, 4]. The study of cancer metabolism dates back to the early 20th century, when Otto Warburg first observed that cancer cells preferentially utilize glycolysis for energy production, even in sufficient oxygen – a phenomenon now known as the Warburg effect [5]. Warburg’s discovery was revolutionary, challenging the prevailing belief that oxidative phosphorylation in mitochondria was the primary energy source for all cells, including cancerous ones. Over the decades, subsequent research has expanded our understanding of the metabolic reprogramming in cancer cells, revealing a complex network of altered pathways that contribute to tumorigenesis and cancer progression.  \nThe metabolic reprogramming in cancer cells is not limited to enhanced glycolysis. It encompasses a range  \nof alterations in vario","cbCaid2juZbMifYo","https://ap.wps.com/l/cbCaid2juZbMifYo","pdf",8254588,"English","# Abstract\n# Introduction\n## Cancer metabolism and the Warburg effect\n## Metabolic pathways and key regulators\n## Therapeutic implications of altered metabolism","[{\"question\":\"What metabolic pathways are highlighted as central to cancer altered metabolism?\",\"answer\":\"The review focuses on glycolysis, oxidative phosphorylation, glutaminolysis, and lipid metabolism, describing how each supports tumor growth and survival.\"},{\"question\":\"How do genes, epigenetics, and the tumor microenvironment affect cancer metabolism?\",\"answer\":\"Oncogenes, tumor suppressors, epigenetic modifications, and the tumor microenvironment coordinate regulation of metabolic pathways to match growth and survival demands.\"},{\"question\":\"Which therapeutic strategies are discussed for targeting cancer metabolism?\",\"answer\":\"The review discusses inhibitors targeting glycolysis enzymes, glutaminolysis, components of the TCA cycle, fatty acid oxidation, LDH, and glucose transport, along with emerging approaches for oxidative phosphorylation and lipid synthesis.\"}]","Altered metabolism in cancer: insights into energy pathways and therapeutic targets | PDF",1789981842,101]