Abstract
Securin is highly-expressed in various tumors including those of the colon. In this study, the role of securin in the anticancer effects of fisetin on human colon cancer cells was investigated. Fisetin-induced apoptosis in HCT116 cells as indicated by TUNEL assay, Annexin V-FITC/PI double staining, Ser15-phosphorylation of p53, and cleavages of procaspase-3 and PARP. These effects were enhanced in HCT116 securin-null cells or in wild-type cells in which securin was knockdown by siRNA, but attenuated when wild-type or non-degradable securin was reconstituted. Moreover, fisetin did not induce apoptosis in HCT116 p53-null and HT-29 p53-mutant cells. Knockdown of securin in HCT116 p53-null cells potentiated fisetin-induced cytotoxicity by induction of apoptosis. Our results provide the first evidence to support that securin depletion sensitizes human colon cancer cells to fisetin-induced apoptosis.
Original language | English |
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Pages (from-to) | 96-104 |
Number of pages | 9 |
Journal | Cancer Letters |
Volume | 300 |
Issue number | 1 |
DOIs | |
Publication status | Published - Jan 1 2011 |
Keywords
- Fisetin
- Human colon cancer cells
- P53
- Securin
ASJC Scopus subject areas
- Oncology
- Cancer Research