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Silencing TAB182 inhibits cell EMT, migration and invasion by downregulating EGFR in A549 NSCLC cells
Shaozheng Wang1, Hejiang Guo1, Jin Jia1,2
1Department of Radiation Toxicology and Oncology, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing, 100850, China.
Background:
TAB182 is overexpressed in cancerous tissues and correlated with poor overall survival in lung cancer patients. Mechanistically, TAB182 participates in DNA damage repair and endows tumour cells with radio- and chemoresistance. However, its role in non-small cell lung cancer (NSCLC) remains unclear.
Methods And Results:
Cells with stable TAB182 knockdown (KD) were generated using A549 NSCLC cells, and we demonstrated that depleting TAB182 inhibits cell EMT, proliferation, colony formation, migration and invasion. Analysis of the TCGA database showed a positive correlation between TAB182 and EGFR, a well-established NSCLC oncoprotein. Then, we verified that silencing TAB182 decreases EGFR expression at both the mRNA and protein levels. Moreover, both TAB182 and EGFR were reported to restore ionizing radiation (IR)-triggered DNA damage. We validated that IR elevates the protein level of EGFR and that silencing TAB182 can alleviate IR-induced EGFR upregulation. Furthermore, overexpressing EGFR abrogates the inhibitory effects of TAB182 KD on EMT, migration, and invasion in A549 cells.
Conclusions:
Our data demonstrated that EGFR expression is regulated by TAB182 and downregulation of TAB182 has a novel function to repress EMT, migration and invasion by decreasing EGFR, indicating TAB182 could regulate the malignant progression of NSCLC.
Insights
TAB182 protein promotes non-small cell lung cancer (NSCLC) progression by increasing epithelial-mesenchymal transition (EMT), migration, and invasion. Downregulating TAB182 inhibits these malignant behaviors by decreasing epidermal growth factor receptor (EGFR) expression.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- TAB182 is overexpressed in cancers and linked to poor survival.
- TAB182 is implicated in DNA repair and treatment resistance.
- The role of TAB182 in non-small cell lung cancer (NSCLC) is not well understood.
Purpose of the Study:
- To investigate the role of TAB182 in NSCLC.
- To explore the relationship between TAB182 and epidermal growth factor receptor (EGFR) in NSCLC.
Main Methods:
- TAB182 knockdown in A549 NSCLC cells.
- Analysis of TCGA database for TAB182 and EGFR correlation.
- Assessment of cell proliferation, EMT, migration, invasion, and colony formation.
- Evaluation of EGFR expression at mRNA and protein levels.
- Investigation of the effects of TAB182 and EGFR on response to ionizing radiation (IR).
Main Results:
- TAB182 knockdown inhibited EMT, proliferation, migration, and invasion in NSCLC cells.
- TAB182 expression positively correlated with EGFR in NSCLC.
- Silencing TAB182 decreased EGFR expression and alleviated IR-induced EGFR upregulation.
- Overexpression of EGFR rescued the inhibitory effects of TAB182 knockdown.
Conclusions:
- TAB182 regulates EGFR expression in NSCLC.
- Downregulation of TAB182 represses NSCLC progression by decreasing EGFR.
- TAB182 plays a significant role in the malignant progression of NSCLC.
