ArticleThe American journal of pathology2001
Protective function of p27(KIP1) against apoptosis in small cell lung cancer cells in unfavorable microenvironments.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 35 citations in OpenAlex.
- Peroxisome Proliferator Activated Receptor Gamma Sensitizes Non-small Cell Lung Carcinoma to Gamma Irradiation Induced Apoptosis.Frontiers in genetics · 2019Article
- New pyrazolo[3,4-d]pyrimidine SRC inhibitors induce apoptosis in mesothelioma cell lines through p27 nuclear stabilization.Oncogene · 2012Article
- Resveratrol protects leukemic cells against cytotoxicity induced by proteasome inhibitors via induction of FOXO1 and p27Kip1.BMC cancer · 2011Article
- MicroRNA-221/222 confers tamoxifen resistance in breast cancer by targeting p27Kip1.The Journal of biological chemistry · 2008Article
- The potential role of pharmacogenomic and genomic in the adjuvant treatment of early stage non small cell lung cancer.Current genomics · 2008Article
- P27kip1 regulates the apoptotic response of gastric epithelial cells to Helicobacter pylori.Gut · 2004Article
- Fludarabine-induced apoptosis of B chronic lymphocytic leukemia cells includes early cleavage of p27kip1 by caspases.Leukemia · 2003Article
- Genetic alterations of multiple tumor suppressors and oncogenes in the carcinogenesis and progression of lung cancer.Oncogene · 2002Review
- Persistent increase in chromosome instability in lung cancer: possible indirect involvement of p53 inactivation.The American journal of pathology · 2001Article
- Role of cell cycle regulators in lung carcinogenesis.Cell adhesion & migrationReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A previous study of ours unexpectedly found that in contrast to frequent reductions in non-small cell lung cancer, high expression of the p27(KIP1) cyclin-dependent kinase (CDK) inhibitor was retained in virtually all small cell lung cancers (SCLCs), suggesting the possibility of high expression of nonfunctional p27(KIP1) in this virulent tumor. The study presented here, however, shows that p27(KIP1) in SCLC biochemically functions as a CDK inhibitor, clearly showing induction apparently associated with G(1)/G(0) arrest and efficient binding to and inhibition of the cyclin E-CDK2 complex. Interestingly, induction of p27(KIP1) 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 p27(KIP1) levels by using a sense p27(KIP1) expression construct or an antisense oligonucleotide supported this notion. These observations suggest that high expression of p27(KIP1) in vivo may favor the survival of SCLC by preventing apoptosis in a microenvironment unfavorable for cell proliferation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.