Cellular models of drug- and radiation-resistant small cell lung cancer.

Abstract

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.

• Authors: Ross A Davey, Vicki L Locke, Sheridan Henness, Rozelle M Harvie, Mary W Davey
• Journal: Anticancer research (Anticancer Res) 2004 Mar-Apr Vol. 24 Issue 2A Pg. 465-71 ISSN: 0250-7005 [Print] Greece
• PMID: 15152945 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antineoplastic Agents, Phytogenic
• CDKN1A protein, human
• Cyclin-Dependent Kinase Inhibitor p21
• Cyclins
• Proto-Oncogene Proteins c-bcl-2
• Proto-Oncogene Proteins c-myc
• Tumor Suppressor Protein p53
• Paclitaxel

Topics

• Antineoplastic Agents, Phytogenic
• Carcinoma, Small Cell (drug therapy, genetics, metabolism, radiotherapy)
• Cell Line, Tumor
• Cyclin-Dependent Kinase Inhibitor p21
• Cyclins (biosynthesis, genetics)
• Drug Resistance, Multiple (drug effects, genetics)
• Drug Resistance, Neoplasm
• Gene Expression (drug effects)
• Genes, bcl-2
• Genes, myc
• Genes, p53
• Humans
• Lung Neoplasms (drug therapy, genetics, metabolism, radiotherapy)
• Paclitaxel (pharmacology)
• Proto-Oncogene Proteins c-bcl-2 (biosynthesis)
• Proto-Oncogene Proteins c-myc (biosynthesis)
• Radiation Tolerance (drug effects, genetics)
• Tumor Suppressor Protein p53 (biosynthesis)