BioMed Research International

BioMed Research International / 2004 / Article

Research article | Open Access

Volume 2004 |Article ID 461360 | https://doi.org/10.1155/S1110724304403131

Abdelali Haoudi, O. John Semmes, James M. Mason, Ronald E. Cannon, "Retrotransposition-Competent Human LINE-1 Induces Apoptosis in Cancer Cells With Intact p53", BioMed Research International, vol. 2004, Article ID 461360, 10 pages, 2004. https://doi.org/10.1155/S1110724304403131

Retrotransposition-Competent Human LINE-1 Induces Apoptosis in Cancer Cells With Intact p53

Received16 Mar 2004
Revised17 Apr 2004
Accepted29 Apr 2004

Abstract

Retrotransposition of human LINE-1 (L1) element, a major representative non-LTR retrotransposon in the human genome, is known to be a source of insertional mutagenesis. However, nothing is known about effects of L1 retrotransposition on cell growth and differentiation. To investigate the potential for such biological effects and the impact that human L1 retrotransposition has upon cancer cell growth, we examined a panel of human L1 transformed cell lines following a complete retrotransposition process. The results demonstrated that transposition of L1 leads to the activation of the p53-mediated apoptotic pathway in human cancer cells that possess a wild-type p53. In addition, we found that inactivation of p53 in cells, where L1 was undergoing retrotransposition, inhibited the induction of apoptosis. This suggests an association between active retrotransposition and a competent p53 response in which induction of apoptosis is a major outcome. These data are consistent with a model in which human retrotransposition is sensed by the cell as a “genetic damaging event” and that massive retrotransposition triggers signaling pathways resulting in apoptosis.

Copyright © 2004 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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