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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
[Effect of EGFR-TKI on lymphangiogenesis of lung cancer with EGFR mutation]
Minghui Cai1, Xinying Yang2, Baohong Jiang2
1Department of Thoracic Cancer, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai Lung Tumor Clinical Medical Center, Shanghai 200030, China.
Background And Objective:
This study aims to explore the effect of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKIs) on the lymphangiogenesis of lung cancer with EGFR mutation, as well as to determine the function of EGFR targeted therapy in relation to the inhibition of lymphangiogenesis during lung cancer treatment.
Methods:
The EGFR double mutant lung cancer cell line NCI-H1975 is used to construct lung cancer xenograft models. The models are divided into two groups: the solvent control group and the EGFR-TKI treatment group. Each group includes five mice. The inhibitory effect of EGFR-TKI on the growth of transplanted tumors was observed. Immunohistochemical method and lymphatic endothelium specific antibody D2-40 were used in the experiment to observe the influence of EGFR-TKI on lymphangiogenesis in lung cancer.
Results:
The weight and relative volume of tumors in the EGFR-TKI treated group were less than those in the solvent control group. The average lymphatic vessel density of EGFR-TKI-treated mice was 6.44 per case. This value was 10.70 per case in the solvent control group. Lower density of lymphangiogenesis was found in the EGFR-TKI treated group (P=0.023). The area and longest diameter of neonatal lymphatic vessel of the EGFR-TKI treated group were less than those of the solvent control group. Moreover, EGFR-TKI exhibited no significant effect on the invasion of tumor cells into the lymphatic vessel (P=0.519).
Conclusions:
EGFR-TKI can inhibit lymphangiogenesis in EGFR mutant lung cancer while suppressing vessel diameter and expansion area.
Insights
Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) effectively reduce lymphangiogenesis in EGFR-mutant lung cancer. This targeted therapy suppresses lymphatic vessel density, diameter, and expansion area, offering a new avenue for lung cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Lung cancer often harbors EGFR mutations, driving tumor growth and metastasis.
- Lymphangiogenesis, the formation of new lymphatic vessels, plays a crucial role in cancer spread.
Purpose of the Study:
- To investigate the impact of EGFR-TKIs on lymphangiogenesis in EGFR-mutant lung cancer.
- To assess the efficacy of EGFR-targeted therapy in inhibiting lung cancer lymphangiogenesis.
Main Methods:
- Utilized NCI-H1975 EGFR double mutant lung cancer cells to create xenograft models.
- Administered EGFR-TKI treatment to assess tumor growth inhibition.
- Employed immunohistochemistry with D2-40 antibody to quantify lymphangiogenesis.
Main Results:
- EGFR-TKI treatment significantly reduced tumor weight and volume compared to controls.
- Lymphatic vessel density was lower in EGFR-TKI treated mice (6.44/case) versus controls (10.70/case).
- EGFR-TKI suppressed lymphatic vessel diameter and expansion area but did not affect tumor cell invasion into vessels.
Conclusions:
- EGFR-TKIs demonstrate potent inhibition of lymphangiogenesis in EGFR-mutant lung cancer.
- Targeted therapy with EGFR-TKIs reduces lymphatic vessel formation and dimensions.
- These findings suggest EGFR-TKIs are valuable in managing lung cancer metastasis via lymphangiogenesis inhibition.
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