DOI QR코드

DOI QR Code

Knockdown of Bcl-3 Inhibits Cell Growth and Induces DNA Damage in HTLV-1-infected Cells)

  • Gao, Cai (Research Center for Immunology, Xinxiang Medical University) ;
  • Wang, Xia (Research Center for Immunology, Xinxiang Medical University) ;
  • Chen, Lin (Research Center for Immunology, Xinxiang Medical University) ;
  • Wang, Jin-Heng (Research Center for Immunology, Xinxiang Medical University) ;
  • Gao, Zhi-Tao (Research Center for Immunology, Xinxiang Medical University) ;
  • Wang, Hui (Research Center for Immunology, Xinxiang Medical University)
  • Published : 2013.01.31

Abstract

Oncoprotein Bcl-3 is perceived as an unusual member of $I{\kappa}B$ family since it can both stimulate and suppress NF-${\kappa}B$ activation. Aberrant Bcl-3 results in increased cell proliferation and survival, suggesting a contribution to malignant potential and elevated levels of Bcl-3 have been observed in many HTLV-1-infected T cell lines and ATL cells. To investigate the specific roles of Bcl-3 in HTLV-1-infected cells, we knocked down Bcl-3 expression using shRNA and then examined the consequences with regard to DNA damage and cell proliferation, as well as NF-${\kappa}B$ activation. The HTLV-1 encoded protein Tax promotes Bcl-3 expression and nuclear translocation. In HTLV-1-infected cells, Bcl-3 knockdown obviously induced DNA damage. Cell growth and NF-${\kappa}B$ activation were reduced in HTLV-1-infected or Tax positive cells when Bcl-3 expression was decreased. Together, our results revealed positive roles of Bcl-3 in DNA stabilization, growth and NF-${\kappa}B$ activation in HTLV-1-infected cells.

Acknowledgement

Supported by : National Natural Science Foundation of China

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