Cancer knocks you out by fasting: Cachexia as a consequence of metabolic alterations in cancer.

IF 4.5 2区 生物学 Q2 CELL BIOLOGY
Salvatore Cortellino, Margherita D'Angelo, Massimiliano Quintiliani, Antonio Giordano
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引用次数: 0

Abstract

Neoplastic transformation reprograms tumor and surrounding host cell metabolism, increasing nutrient consumption and depletion in the tumor microenvironment. Tumors uptake nutrients from neighboring normal tissues or the bloodstream to meet energy and anabolic demands. Tumor-induced chronic inflammation, a high-energy process, also consumes nutrients to sustain its dysfunctional activities. These tumor-related metabolic and physiological changes, including chronic inflammation, negatively impact systemic metabolism and physiology. Furthermore, the adverse effects of antitumor therapy and tumor obstruction impair the endocrine, neural, and gastrointestinal systems, thereby confounding the systemic status of patients. These alterations result in decreased appetite, impaired nutrient absorption, inflammation, and shift from anabolic to catabolic metabolism. Consequently, cancer patients often suffer from malnutrition, which worsens prognosis and increases susceptibility to secondary adverse events. This review explores how neoplastic transformation affects tumor and microenvironment metabolism and inflammation, leading to poor prognosis, and discusses potential strategies and clinical interventions to improve patient outcomes.

癌症通过禁食将你击倒:癌症新陈代谢改变导致的恶病质。
肿瘤转化会重塑肿瘤和周围宿主细胞的新陈代谢,增加肿瘤微环境中的营养消耗和耗竭。肿瘤从邻近的正常组织或血液中吸收营养物质,以满足能量和合成代谢的需求。肿瘤诱发的慢性炎症是一个高能量过程,也会消耗营养物质以维持其功能紊乱的活动。这些与肿瘤相关的代谢和生理变化,包括慢性炎症,对全身代谢和生理产生了负面影响。此外,抗肿瘤治疗的不良反应和肿瘤阻塞损害了内分泌、神经和胃肠系统,从而混淆了患者的全身状况。这些改变导致食欲下降、营养吸收障碍、炎症以及从合成代谢到分解代谢的转变。因此,癌症患者常常营养不良,从而使预后恶化,并增加了继发性不良事件的易感性。本综述探讨了肿瘤转化如何影响肿瘤和微环境代谢及炎症,从而导致不良预后,并讨论了改善患者预后的潜在策略和临床干预措施。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
14.70
自引率
0.00%
发文量
256
审稿时长
1 months
期刊介绍: The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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