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Updated: Aug 24, 2026
Radiosensitivity of Cancer Stem Cells in Lung Cancer Cell Lines
Published on: August 21, 2019
Cellular models of drug- and radiation-resistant small cell lung cancer
Ross A Davey1, Vicki L Locke, Sheridan Henness
1Bill Walsh Cancer Research Laboratories, Royal North Shore Hospital, St Leonards NSW 2065, Australia. rdavey@med.usyd.edu.au
Background:
The H69-EPR, H69-CP, H69-VP and H69/R38 resistant sublines of the classic small cell lung cancer (SCLC) line have proven useful in studies of resistance and its circumvention with paclitaxel.
Materials And Methods:
The suppressor/oncogene profile of these sublines determined by Western and Northern blot was compared to the variant H82 SCLC cell profile. Two-dimensional electrophoresis/mass spectrometry was used to determine the effect of paclitaxel on protein expression.
Results:
The H69-EPR and H69-CP resistant sublines were similar to the variant H82 cells for bcl-2, p21waf1, p53, N-myc and c-myc expression while the H69-VP subline retained the classic H69 pattern. A 1-h treatment with 10 ng/ml paclitaxel substantially reversed the resistance except for the H69/R38 subline and tended to reverse the resistance-associated changes in protein expression in the H69-EPR subline.
Conclusion:
Although some resistant sublines express a variant pattern of suppressor/oncogenes with low bcl-2, resistance is substantially reversed by paclitaxel treatment.
Insights
Paclitaxel treatment significantly reverses drug resistance in small cell lung cancer (SCLC) cell lines, restoring normal suppressor/oncogene profiles. This finding offers hope for overcoming treatment resistance in SCLC patients.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Established small cell lung cancer (SCLC) cell lines (H69-EPR, H69-CP, H69-VP, H69/R38) were utilized to study paclitaxel resistance.
- These resistant sublines provide a model for investigating mechanisms of drug resistance and potential circumvention strategies.
Purpose of the Study:
- To compare the suppressor/oncogene profiles of paclitaxel-resistant SCLC sublines with a variant SCLC cell line (H82).
- To investigate the effect of paclitaxel treatment on protein expression in these resistant SCLC sublines.
Main Methods:
- Western blot and Northern blot analyses were performed to determine suppressor/oncogene profiles.
- Two-dimensional electrophoresis coupled with mass spectrometry was employed to assess protein expression changes following paclitaxel treatment.
Main Results:
- Resistant sublines H69-EPR and H69-CP exhibited similar bcl-2, p21waf1, p53, N-myc, and c-myc expression patterns to the variant H82 cells.
- The H69-VP subline maintained the original H69 cell expression pattern.
- A short paclitaxel treatment (1 hour at 10 ng/ml) substantially reversed resistance in most sublines, except for H69/R38, and tended to reverse resistance-associated protein expression changes in H69-EPR.
Conclusions:
- Despite some resistant sublines displaying a variant suppressor/oncogene profile with low bcl-2 expression, paclitaxel treatment effectively reverses this resistance.
- Paclitaxel demonstrates potential in overcoming drug resistance in SCLC, highlighting its therapeutic value.
