Results describe a previously unrecognized, SCFskp2-independent role for the control of p27 mRNA abundance in the development of non-small cell lung cancers.

p27 is a potent barrier to the growth and malignant progression of Kras-initiated lung tumors.

Cytoplasmic p27(Kip1) promotes tumorigenesis by suppressing RhoB activity in non-small cell lung carcinoma cells.

Skp2 mRNA expression level was high in squamous cell carcinomas of the lung and was inversely related with the p27(Kip1) protein level

Inhibition of thromboxan synthase TXS results in the p27-related induction of cell death in lung cancer cells.

Overexpressions of nuclear p27 is associated with non-small cell lung cancer.

FoxM1, p27(kip1) and p21(waf1/cip1) showed distinct immunoreactivity according to histological subtype, which may help in the differential diagnosis of pulmonary neuroendocrine tumours.

miR-194 suppresses metastasis of non-small cell lung cancer through regulating expression of BMP1 and p27kip1

miR-340 controls p27 at both translational and posttranslational levels in non-small cell lung cancer

in lung cancer tissues, upregulation of mdig expression accompanies with the downregulation of p27(KIP1) expression and in bronchial stump

Data show that cytoplasmic cyclin-dependent kinase inhibitor p27 is preferentially observed in primary non-small cell lung cancer (NSCLC) with activated proto-oncogene proteins c-akt1 and predicts poor survival.

A novel lncRNA, LUADT1, promotes lung adenocarcinoma proliferation via the epigenetic suppression of p27.

cytoplasmic p27, via ERK-activated Bcl-2 expression may predict an unfavorable response to cisplatin-based chemotherapy and poor outcomes in non-small cell lung cancer.

Dsg2 knockdown arrests non-small cell lung cancer cell cycle progression via modulation of p27-CDK2 levels.

ACTB, CDKN1B, GAPDH, GRB2, RHOA and SDCBP are potent reference genes in neuroendocrine tumors of the lung.

Low P27KIP1 expression is associated with Non Small Cell lung cancer.

p27 and its cognate ubiquitin ligases, Skp2/KPC/Pirh2, are specifically involved in determining the clinical profiles of lung carcinomas.

Taken together, these data clearly show that FKBP3/Sp1/HDAC2/p27 control cell proliferation during non-small cell lung cancer development.

These results demonstrated that JSK could trigger cell cycle arrest at the G2/M phase and apoptosis in A549 and H460 cells, which was likely mediated via the p53/p21WAF1/CIP1 and p27KIP1 pathways. Overall, the results indicated that JSK may be used as an anticancer agent for the treatment of nonsmall cell lung cancer (NSCLC)