Cargill Kasey R, Hasken William L, Gay Carl M, Byers Lauren A
Department of Thoracic/Head and Neck Medical Oncology, University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Front Oncol. 2021 Oct 21;11:757323. doi: 10.3389/fonc.2021.757323. eCollection 2021.
Metabolic reprogramming is a hallmark of cancer initiation, progression, and relapse. From the initial observation that cancer cells preferentially ferment glucose to lactate, termed the Warburg effect, to emerging evidence indicating that metabolic heterogeneity and mitochondrial metabolism are also important for tumor growth, the complex mechanisms driving cancer metabolism remain vastly unknown. These unique shifts in metabolism must be further investigated in order to identify unique therapeutic targets for individuals afflicted by this aggressive disease. Although novel therapies have been developed to target metabolic vulnerabilities in a variety of cancer models, only limited efficacy has been achieved. In particular, lung cancer metabolism has remained relatively understudied and underutilized for the advancement of therapeutic strategies, however recent evidence suggests that lung cancers have unique metabolic preferences of their own. This review aims to provide an overview of essential metabolic mechanisms and potential therapeutic agents in order to increase evidence of targeted metabolic inhibition for the treatment of lung cancer, where novel therapeutics are desperately needed.
代谢重编程是癌症起始、进展和复发的一个标志。从最初观察到癌细胞优先将葡萄糖发酵为乳酸(即瓦伯格效应),到新出现的证据表明代谢异质性和线粒体代谢对肿瘤生长也很重要,驱动癌症代谢的复杂机制仍大多未知。必须进一步研究这些独特的代谢变化,以便为受这种侵袭性疾病折磨的个体确定独特的治疗靶点。尽管已经开发出针对多种癌症模型中代谢脆弱性的新型疗法,但仅取得了有限的疗效。特别是,肺癌代谢相对较少受到研究,在治疗策略的推进中也未得到充分利用,然而最近的证据表明肺癌有其自身独特的代谢偏好。本综述旨在概述基本的代谢机制和潜在的治疗药物,以增加针对肺癌治疗的靶向代谢抑制的证据,因为目前迫切需要新型疗法。