Evolution from genetics to phenotype: reinterpretation of NSCLC plasticity, heterogeneity, and drug resistance.
10.1007/s13238-016-0330-1
- Author:
Yingjiao XUE
1
;
Shenda HOU
1
;
Hongbin JI
1
;
Xiangkun HAN
2
Author Information
1. Key Laboratory of Systems Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
2. Key Laboratory of Systems Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China. xkhan@sibs.ac.cn.
- Publication Type:Journal Article
- Keywords:
drug resistance;
heterogeneity;
lung cancer;
phenotypic transition;
plasticity
- MeSH:
Carcinoma, Non-Small-Cell Lung;
genetics;
metabolism;
Drug Resistance, Neoplasm;
genetics;
Humans;
Lung Neoplasms;
genetics;
metabolism
- From:
Protein & Cell
2017;8(3):178-190
- CountryChina
- Language:English
-
Abstract:
Lung cancer is the leading cause of cancer-related deaths worldwide. Targeted therapy is beneficial in most cases, but the development of drug resistance stands as an obstacle to good prognosis. Multiple mechanisms were explored such as genetic alterations, activation of bypass signaling, and phenotypic transition. These intrinsic and/or extrinsic dynamic regulations facilitate tumor cell survival in meeting the demands of signaling under different stimulus. This review introduces lung cancer plasticity and heterogeneity and their correlation with drug resistance. While cancer plasticity and heterogeneity play an essential role in the development of drug resistance, the manipulation of them may bring some inspirations to cancer prognosis and treatment. That is to say, lung cancer plasticity and heterogeneity present us with not only challenges but also opportunities.
