Induction of cell apoptosis in non-small cell lung cancer cells by cyclin A1 small interfering RNA

Cancer Sci. 2006 Oct;97(10):1082-92. doi: 10.1111/j.1349-7006.2006.00292.x.


Cyclin A1 and cyclin B1 are overexpressed in various tumors but are present at low levels in normal tissues. Cyclin A1 is restricted to germ cells undergoing meiosis. In order to explore the possibility of using cyclin A1 and cyclin B1 as anticancer targets, we knocked them down in two lung cancer cell lines, H157 and H596, using siRNA. As with cyclin A1 siRNA in lung cancer cell lines, cyclin B1, Cdc2 and CDK2 were all significantly downregulated. The S phase fraction increased significantly, and they eventually underwent apoptosis by way of downregulated intrinsic apoptotic pathways and modulators with upregulated extrinsic apoptotic pathways. Our study suggests that cyclin A1 might be a promising anticancer target specific to lung cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis* / genetics
  • Carcinoma, Non-Small-Cell Lung / genetics*
  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Cell Cycle / genetics
  • Cell Proliferation / drug effects
  • Cyclin A / antagonists & inhibitors*
  • Cyclin A / genetics
  • Cyclin A / metabolism
  • Cyclin A1
  • Gene Expression Profiling
  • Humans
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / metabolism
  • RNA, Small Interfering / pharmacology*
  • Tumor Cells, Cultured


  • CCNA1 protein, human
  • Cyclin A
  • Cyclin A1
  • RNA, Small Interfering