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From the Divisions of Molecular Oncology*
and
Immunology,§
Aichi Cancer Center Research
Institute, Nagoya; and the Departments of Pathology and Clinical
Laboratories
and Pulmonary
Medicine,
Aichi Cancer Center Hospital,
Nagoya, Japan
A previous study of ours unexpectedly found that in contrast to frequent reductions in non-small cell lung cancer, high expression of the p27KIP1 cyclin-dependent kinase (CDK) inhibitor was retained in virtually all small cell lung cancers (SCLCs), suggesting the possibility of high expression of nonfunctional p27KIP1 in this virulent tumor. The study presented here, however, shows that p27KIP1 in SCLC biochemically functions as a CDK inhibitor, clearly showing induction apparently associated with G1/G0 arrest and efficient binding to and inhibition of the cyclin E-CDK2 complex. Interestingly, induction of p27KIP1 seems to confer on SCLC cells the ability to survive under culture conditions unfavorable for cell growth such as a lack of nutrients and hypoxia. Subsequent experiments manipulating p27KIP1 levels by using a sense p27KIP1 expression construct or an antisense oligonucleotide supported this notion. These observations suggest that high expression of p27KIP1 in vivo may favor the survival of SCLC by preventing apoptosis in a microenvironment unfavorable for cell proliferation.
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