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[Cancer Research 56, 4856-4861, November 1, 1996]
© 1996 American Association for Cancer Research
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Flavopiridol: A Cytotoxic Flavone That Induces Cell Death in Noncycling A549 Human Lung Carcinoma Cells1

Keith C. Bible2 and Scott H. Kaufmann

Division of Oncology Research, Mayo Clinic, and Department of Pharmacology, Mayo Medical School, Rochester, Minnesota 55905

Flavopiridol (NSC 649890, L86-8275), a potent inhibitor of cyclin-dependent kinase 1/p34cdc2 phosphorylation and kinase activity, is currently undergoing Phase I clinical testing as a potential antineoplastic agent. Previous studies have suggested that flavopiridol is cytostatic but not cytotoxic when applied to exponentially growing cells. In the present study, various human tumor cell lines were assayed for trypan blue exclusion and ability to form colonies after exposure to flavopiridol under a variety of growth conditions. When log phase A549 non-small cell lung cancer cells were examined 72 h after the start of a 24-h flavopiridol exposure, as many as 90% of the cells accumulated trypan blue. A 24-h exposure to 250–300 nM resulted in trypan blue uptake in 50% of A549 cells at 72 h and a 50% reduction in colony formation. Similar results were observed in HCT8 ileocecal adenocarcinoma, T98G glioblastoma, MCF-7 breast adenocarcinoma, and HL-60 leukemia cells. With A549 cells, identical results were obtained in actively growing logarithmic phase cells and growth-arrested confluent cells. Treatment with the DNA synthesis inhibitor aphidicolin only minimally affected the cytotoxicity of flavopiridol. In contrast, the RNA synthesis inhibitor 5,6-dichloro-1-ß-D-ribofuranosyl-benzimidazole or the protein synthesis inhibitor cycloheximide reduced the cytotoxicity of flavopiridol. These results suggest that: (a) flavopiridol is not only cytostatic, but also cytotoxic to a variety of human tumor cell lines; (b) flavopiridol is equally active against cycling and noncycling A549 cells; and (c) RNA and protein synthesis appear to play a role in flavopiridol-induced cytotoxicity.

1 This work was supported in part by NIH Grants U01 CA66912 and U01 CA66084.

2 To whom requests for reprints should be addressed, at Division of Oncology Research, Mayo Clinic, 200 First Street S.W., Rochester, MN 55905. Phone: (507) 284-8950; Fax: (507) 284-3906.

Received 7/29/96. Accepted 9/17/96.




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