Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5505563 | Biochemical and Biophysical Research Communications | 2017 | 8 Pages |
Abstract
We show here that ectopic expression of the CDK inhibitor p21Cip1 enhanced deregulated E2F activity and pro-apoptotic E2F target gene expression in cancer cells. Moreover, ectopic expression of p21Cip1 augmented cancer specific cytotoxicity of Ad-ARF-TK, and apoptosis induced by p21Cip1 was dependent on deregulated E2F activity. These results suggest that p21Cip1 specifically enhances deregulated E2F activity and that a combination of the CDK inhibitor with Ad-ARF-TK could be effectively employed for cancer therapy.
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Authors
Kenta Kurayoshi, Ayumi Shiromoto, Eiko Ozono, Ritsuko Iwanaga, Andrew P. Bradford, Keigo Araki, Kiyoshi Ohtani,