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Transcriptional activation of the proapoptotic bik gene by E2F proteins in cancer cells
Author(s) -
Real Pedro J.,
Sanz Cristina,
Gutierrez Olga,
Pipaon Carlos,
Zubiaga Ana M.,
Fernandez-Luna Jose L.
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.08.088
Subject(s) - e2f , apoptosis , programmed cell death , cancer cell , gene , cancer research , microbiology and biotechnology , gene expression , biology , cell cycle , cancer , chemistry , genetics
BH3‐only proteins are required for execution of apoptotic cell death. We have found that one of these proteins, Bik, is strongly induced in cancer cells treated with chemotherapeutic agents. Furthermore, we showed that chemotherapy‐induced expression of bik is independent of p53. Consistent with its pro‐apoptotic activity, blockade of bik expression reduces the adriamycin‐mediated apoptotic cell death. We also found that the bik gene is transcriptionally activated by E2F proteins. Consistently, adriamycin induces the E2F‐bik pathway. In addition, E2Fs transactivate bik by a p53‐independent mechanism. Thus, our data indicate that transcriptional regulation of bik contributes to the efficient apoptotic response to chemotherapeutic agents.