Role of metabolic reprogramming in drug resistance to epidermal growth factor tyrosine kinase inhibitors in non-small cell lung cancer.
10.11817/j.issn.1672-7347.2021.200529
- Author:
Yu WU
1
;
Wei GAO
2
,
3
;
Hao LIU
4
Author Information
1. Department of Pharmacology, School of Pharmacy, Bengbu Medical College; Anhui Provincial Biochemical Drugs Engineering Technology Research Center, Bengbu Anhui 233030, China. a147wu@foxmail.com.
2. Department of Pharmacology, School of Pharmacy, Bengbu Medical College; Anhui Provincial Biochemical Drugs Engineering Technology Research Center, Bengbu Anhui 233030, China. gaowei722@
3. com.
4. Department of Pharmacology, School of Pharmacy, Bengbu Medical College; Anhui Provincial Biochemical Drugs Engineering Technology Research Center, Bengbu Anhui 233030, China. liuhao6886@foxmail.com.
- Publication Type:Journal Article
- Keywords:
drug resistance;
epiderinal growth factor receptor tyrosine kinase inhibitor;
non-small cell lung cancer;
tumor metabolism reprogramming
- MeSH:
Carcinoma, Non-Small-Cell Lung/genetics*;
Cell Line, Tumor;
Drug Resistance, Neoplasm/genetics*;
Epidermal Growth Factor;
ErbB Receptors/genetics*;
Humans;
Lung Neoplasms/genetics*;
Mutation;
Protein Kinase Inhibitors/therapeutic use*;
Tumor Microenvironment
- From:
Journal of Central South University(Medical Sciences)
2021;46(5):545-551
- CountryChina
- Language:English
-
Abstract:
Epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) can effectively inhibit the growth of EGFR-dependent mutant non-small cell lung cancer (NSCLC). Unfortunately, NSCLC patients often develop severe drug resistance after long-term EGFR-TKI treatment. Studies have shown that the disorder of energy metabolism in tumor cells can induce EGFR-TKI resistance. Due to the drug action, gene mutation and other factors, tumor cells undergo metabolic reprogramming, which increases the metabolic rate and intensity of tumor cells, promotes the intake and synthesis of nutrients (such as sugar, fat and glutamine), forms a microenvironment conducive to tumor growth, enhances the bypass activation, phenotype transformation and abnormal proliferation of tumor cells, and inhibits the activity of immune cells and apoptosis of tumor cells, ultimately leading to drug resistance of tumor cells to EGFR-TKI. Therefore, targeting energy metabolism of NSCLC may be a potential way to alleviate TKI resistance.
