Metabolic reprogramming by tobacco-specific nitrosamines (TSNAs) in cancer

被引:28
作者
Sarlak, Saharnaz [1 ,2 ]
Lalou, Claude [1 ,2 ]
Amoedo, Nivea Dias [3 ]
Rossignol, Rodrigue [1 ,2 ,3 ]
机构
[1] INSERM, U1211, F-33000 Bordeaux, France
[2] Bordeaux Univ, 146 Rue Leo Saignat, F-33000 Bordeaux, France
[3] CELLOMET, Funct Genom Ctr CGFB, 146 Rue Leo Saignat, F-33000 Bordeaux, France
基金
欧盟地平线“2020”;
关键词
NICOTINIC ACETYLCHOLINE-RECEPTORS; BINDING PROTEIN CREB; MOUSE LUNG ADENOCARCINOMAS; BETA-ADRENERGIC-RECEPTORS; CIGARETTE-SMOKE EXPOSURE; GROWTH-FACTOR RECEPTOR; FATTY-ACID OXIDATION; NEURAL STEM-CELLS; F344; RATS; GENE-EXPRESSION;
D O I
10.1016/j.semcdb.2019.09.001
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Metabolic reprogramming is a hallmark of cancer and the link between oncogenes activation, tumor supressors inactivation and bioenergetics modulation is well established. However, numerous carcinogenic environmental factors are responsible for early cancer initiation and their impact on metabolic reprogramming just starts to be deciphered. For instance, it was recently shown that UVB irradiation triggers metabolic reprogramming at the pre-cancer stage with implication for skin cancer detection and therapy. These observations foster the need to study the early changes in tissue metabolism following exposure to other carcinogenic events. According to the International Agency for Research on Cancer (IARC), tobacco smoke is a major class I-carcinogenic environmental factor that contains different carcinogens, but little is known on the impact of tobacco smoke on tissue metabolism and its participation to cancer initiation. In particular, tobacco-specific nitrosamines (TSNAs) play a central role in tobacco-smoke mediated cancer initiation. Here we describe the recent advances that have led to a new hypothesis regarding the link between nitrosamines signaling and metabolic reprogramming in cancer.
引用
收藏
页码:154 / 166
页数:13
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