Asian Pacific Journal of Cancer Prevention

Asian Pacific Journal of Cancer Prevention (아시아태평양암예방학회)
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Suppression of Cellular Apoptosis Susceptibility (CSE1L) Inhibits Proliferation and Induces Apoptosis in Colorectal Cancer Cells

  • Zhu, Jin-Hui (Department of General Surgery and Laparoscopic Center, Second Affiliated Hospital, Zhejiang University School of Medicine) ;
  • Hong, De-Fei (Department of Hepatobiliarypancreatic Surgery, Zhejiang Province People's Hospital) ;
  • Song, Yong-Mao (Department of Surgical Oncology, Second Affiliated Hospital, Zhejiang University School of Medicine) ;
  • Sun, Li-Feng (Department of Surgical Oncology, Second Affiliated Hospital, Zhejiang University School of Medicine) ;
  • Wang, Zhi-Fei (Department of Hepatobiliarypancreatic Surgery, Zhejiang Province People's Hospital) ;
  • Wang, Jian-Wei (Department of Surgical Oncology, Second Affiliated Hospital, Zhejiang University School of Medicine)
  • Published : 2013.02.28
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Abstract

The cellular apoptosis susceptibility (CSE1L) gene has been demonstrated to regulate multiple cellular mechanisms including the mitotic spindle check point as well as proliferation and apoptosis. However, the importance of CSE1L in human colon cancer is largely unknown. In the present study, we examined expression levels of CSE1L mRNA by semiquantitative RT-PCR. A lentivirus-mediated small interfering RNA (siRNA) was used to knock down CSE1L expression in the human colon cancer cell line RKO. Changes in CSE1L target gene expression were determined by RT-PCR. Cell proliferation was examined by a high content screening assay. In vitro tumorigenesis was measured by colony-formation assay. Cell cycle distribution and apoptosis were detected by flow cytometric analysis. We found CSE1L mRNA to be expressed in human colon cancer cells. Using a lentivirus based RNAi approach, CSE1L expression was significantly inhibited in RKO cells, causing cell cycle arrest in the G2/M and S phases and a delay in cell proliferation, as well as induction of apoptosis and an inhibition of colony growth capacity. Collectively, the results suggest that silencing of CSE1L may be a potential therapeutic approach for colon cancer.

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References

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