Metabolic Remodelling: An Accomplice for New Therapeutic Strategies to Fight Lung Cancer

被引:12
|
作者
Mendes, Cindy [1 ,2 ]
Serpa, Jacinta [1 ,2 ]
机构
[1] Univ Nova Lisboa, Fac Ciencias Med, NOVA Med Sch, CEDOC,Chron Dis Res Ctr, Campo Martires Patria 130, P-1169056 Lisbon, Portugal
[2] IPOLFG, Rua Prof Lima Basto, P-1099023 Lisbon, Portugal
关键词
lung cancer; cancer metabolism; reactive oxygen species (ROS); therapy resistance; new therapeutic strategies; GROWTH-FACTOR RECEPTOR; GLUTATHIONE-S-TRANSFERASE; INDUCIBLE FACTOR 1-ALPHA; CISPLATIN RESISTANCE; DRUG-RESISTANCE; ACQUIRED-RESISTANCE; CELL-LINE; IN-VITRO; MULTIDRUG-RESISTANCE; DNA-REPAIR;
D O I
10.3390/antiox8120603
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Metabolic remodelling is a hallmark of cancer, however little has been unravelled in its role in chemoresistance, which is a major hurdle to cancer control. Lung cancer is a leading cause of death by cancer, mainly due to the diagnosis at an advanced stage and to the development of resistance to therapy. Targeted therapeutic agents combined with comprehensive drugs are commonly used to treat lung cancer. However, resistance mechanisms are difficult to avoid. In this review, we will address some of those therapeutic regimens, resistance mechanisms that are eventually developed by lung cancer cells, metabolic alterations that have already been described in lung cancer and putative new therapeutic strategies, and the integration of conventional drugs and genetic and metabolic-targeted therapies. The oxidative stress is pivotal in this whole network. A better understanding of cancer cell metabolism and molecular adaptations underlying resistance mechanisms will provide clues to design new therapeutic strategies, including the combination of chemotherapeutic and targeted agents, considering metabolic intervenients. As cancer cells undergo a constant metabolic adaptive drift, therapeutic regimens must constantly adapt.
引用
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页数:25
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