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M. Morise
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P1.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 233)
- Event: WCLC 2015
- Type: Poster
- Track: Biology, Pathology, and Molecular Testing
- Presentations: 1
- Moderators:
- Coordinates: 9/07/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P1.04-065 - Cyclin-Dependent kinase11 (CDK11) Is Crucial for Growth of Lung Cancer Cells (ID 877)
09:30 - 09:30 | Author(s): M. Morise
- Abstract
Background:
Cyclin dependent kinases (CDKs) are protein kinases that regulate cell growth and proliferation in cells. CDK11 belongs to transcriptional subfamilies of CDKs and has been reported to be crucial for survival of sarcoma and breast cancer cells. To examine its roles in lung cancer cells, we investigated the effect of CDK11 knockdown on non-small cell lung cancer (NSCLC) cell lines.
Methods:
17 NSCLC cell lines were used for expression analysis of CDK11. Among them, we used three lung cancer cell lines, H460, H1299 and H358 for functional analysis. Synthetic siRNAs were utilized to knockdown CDK11. mRNA and protein levels of CDK11 were evaluated by real-time PCR and western blotting, respectively. Changes in growth were examined by WST-1 proliferation assay and liquid and soft agar colony formation assays. Cell cycle and apoptosis were analyzed by FACS with propidium iodide staining.
Results:
Western blot analysis revealed that all of the 17 lung cancer cell lines expressed CDK11 mRNA and protein and that compared to a normal cell line, H460 expressed CDK11 at lower levels but H1299 and H358 expressed CDK11 at higher levels. CDK11 knockdown suppressed proliferation and anchorage-dependent and independent clonal growth in H460 and H1299 cell lines but not in H358. Induction of apoptosis was seen in H460 but not in the others.
Conclusion:
CDK11 knockdown suppressed proliferation and clonogenic growth in H460 and H1299 cells, and induced apoptosis in H460. These results suggest that inhibiting CDK11 may be an attractive target for the treatment of NSCLC.