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Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
Published on: August 11, 2017
Downregulation of caveolin-1 increased EGFR-TKIs sensitivity in lung adenocarcinoma cell line with EGFR mutation
Yujie Cui1, Tienian Zhu2, Xuejing Song3
1Department of Oncology, Hebei Medical University, Shijiazhuang 050017, Hebei, China; Department of Oncology, Hebei Genenral Hospital, Shijiazhuang 050051, Hebei, China.
Abstract:
Although epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), including gefitinib and erlotinib, have shown notable effects in lung adenocarcinoma patients harboring EGFR mutations, there are significant differences between individual patients in the degree of benefits provided by EGFR-TKIs. Some evidence supports a role for caveolin-1 (Cav-1) in modulating drug sensitivity. This study aimed to investigate whether Cav-1 plays an important role in sensitivity to EGFR-TKIs in lung adenocarcinoma cells. Downregulation of Cav-1 in PC-9 cells were performed to investigate changes in sensitivity to EGFR-TKIs in vitro and in vivo. Knockdown of Cav-1 dramatically enhanced sensitivity to EGFR-TKIs by down-regulating phosphorylation of EGFR. These results suggest that Cav-1 may be a predictor of the poor efficacy of EGFR-TKIs treatment in lung adenocarcinoma with EGFR mutations.
Insights
Caveolin-1 (Cav-1) downregulation enhances sensitivity to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) in lung adenocarcinoma. This suggests Cav-1 may predict poor response to EGFR-TKIs in patients with EGFR mutations.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are effective against lung adenocarcinoma with EGFR mutations.
- Patient response to EGFR-TKIs varies significantly.
- Caveolin-1 (Cav-1) is implicated in drug sensitivity modulation.
Purpose of the Study:
- To investigate the role of Cav-1 in EGFR-TKI sensitivity in lung adenocarcinoma cells.
- To determine if Cav-1 influences the efficacy of EGFR-TKIs.
Main Methods:
- Downregulation of Cav-1 in PC-9 lung adenocarcinoma cells.
- In vitro and in vivo assessment of sensitivity to EGFR-TKIs.
- Analysis of EGFR phosphorylation levels.
Main Results:
- Knockdown of Cav-1 significantly increased sensitivity to EGFR-TKIs.
- Cav-1 downregulation led to decreased phosphorylation of EGFR.
- These findings were observed in both in vitro and in vivo models.
Conclusions:
- Caveolin-1 downregulation enhances EGFR-TKI efficacy in lung adenocarcinoma.
- Cav-1 may serve as a predictive biomarker for poor response to EGFR-TKIs in lung adenocarcinoma patients with EGFR mutations.
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