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Updated: Mar 30, 2026
Radiosensitivity of Cancer Stem Cells in Lung Cancer Cell Lines
Published on: August 21, 2019
Endostatin exerts radiosensitizing effect in non-small cell lung cancer cells by inhibiting VEGFR2 expression
Background:
To determine the effects of endostatin on vascular growth factor receptor 2 (VEGFR2) expression in non-small cell lung cancer (NSCLC) cells and the mechanisms underlying its radiosensitizing effect.
Methods:
VEGFR2 mRNA levels were determined in different NSCLC cell lines using qRT-PCR. RT-PCR and Western blot assays were used to assess the expression of mRNA and proteins. The radiosensitivity of the cells was determined by colony-formation assays; and cell apoptosis and cell cycle distribution were determined by flow cytometry.
Results:
VEGFR2 mRNA levels differed among the five NSCLC cell lines (P < 0.01), with the highest expression in Calu-1 cells and lowest in A549 cells. Endostatin significantly inhibited the growth of Calu-1 cells (P < 0.01) (IC20 = 296.5 μg/ml), and the expression of VEGFR2 and HIF-1α (P < 0.05). Phosphorylation of protein kinase B (Akt), extracellular signal-regulated kinases 1/2 (ERK1/2), and p38 were significantly lower in endostatin-treated cells than control (P < 0.05). Endostatin enhanced the radiosensitivity of Calu-1 cells to SER = 1.38 and induced apoptosis (P < 0.01) and G2/M blockage (P < 0.01). However, endostatin had limited effects on A549 cells. Compared with Calu-1 cells, there was not significantly effects on cell radiosensitivity (SER = 1.09).
Conclusions:
Endostatin induces apoptosis and enhances radiosensitivity of the VEGFR2 high-expressing cell line Calu-1, but it has a limited effect on the VEGFR2 low-expressing cell line A549.
Insights
Endostatin enhances radiosensitivity in non-small cell lung cancer (NSCLC) cells with high vascular growth factor receptor 2 (VEGFR2) expression by inducing apoptosis. It has limited effects on NSCLC cells with low VEGFR2 expression.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Investigating endostatin's impact on vascular growth factor receptor 2 (VEGFR2) in non-small cell lung cancer (NSCLC).
- Understanding the mechanisms behind endostatin's radiosensitizing effects in NSCLC.
Purpose of the Study:
- To determine endostatin's effects on VEGFR2 expression in NSCLC cells.
- To elucidate the mechanisms of endostatin's radiosensitizing properties.
Main Methods:
- Quantitative reverse transcription PCR (qRT-PCR) for VEGFR2 mRNA levels.
- Western blot and RT-PCR for gene and protein expression.
- Colony-formation assays for radiosensitivity.
- Flow cytometry for apoptosis and cell cycle analysis.
Main Results:
- VEGFR2 mRNA levels varied significantly among NSCLC cell lines.
- Endostatin inhibited Calu-1 cell growth and reduced VEGFR2 and HIF-1α expression.
- Endostatin enhanced radiosensitivity in Calu-1 cells, inducing apoptosis and G2/M cell cycle arrest.
- Limited effects of endostatin were observed in A549 cells with low VEGFR2 expression.
Conclusions:
- Endostatin promotes apoptosis and enhances radiosensitivity in VEGFR2-high NSCLC cells (Calu-1).
- Endostatin exhibits limited efficacy in VEGFR2-low NSCLC cells (A549).
