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RNA Silencing of Cks1 Induced G2/M Arrest and Apoptosis in Human Lung Cancer Cells
Author(s) -
Tsai YiShan,
Chang HuiChiu,
Chuang LeaYea,
Hung WenChun
Publication year - 2005
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216540500215531
Subject(s) - carcinogenesis , small interfering rna , lung cancer , cancer research , transfection , microbiology and biotechnology , kinase , cyclin dependent kinase 1 , biology , gene silencing , apoptosis , cell cycle , cancer , chemistry , cell culture , medicine , pathology , gene , biochemistry , genetics
Cdc kinase subunit 1 (Cks1) has been shown to involve in the regulation of cell cycle progression and p27Kip1 degradation. To define the role of Cks1 in lung tumorigenesis, we examined the expression of Cks1 in human lung cancer cell lines and tested the effect of Cks1‐specific small interfering RNA (siRNA) on these cells. Reverse transcriptase‐polymerase chain reaction (RT‐PCR) and western blot analysis showed that Cks1 was highly expressed in human lung cancer cells. Transfection of Cks1 siRNA down‐regulated Cdc2 kinase activity and induced G2/M arrest in Cks1‐ overexpressing H358 lung cancer cells. Long‐term treatment of Cks1 siRNA induced caspase activation and apoptosis in H358 cells. On the contrary, Cks1 siRNA did not affect viability of normal human lung fibroblasts under the same experimental condition. Collectively, our results suggest that Cks1 participates in the steps of lung tumorigenesis and this gene may be a target for the treatment of lung cancer.IUBMB Life, 57: 583‐589, 2005