The effects of phenoxodiol on the cell cycle of prostate cancer cell lines
Background: Prostate cancer is associated with a poor survival rate. The ability of cancer cells to evade apoptosis and exhibit limitless replication potential allows for progression of cancer from a benign to a metastatic phenotype. The aim of this study was to investigate in vitro the effect of th...
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| Format: | Journal Article |
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BioMed Central Ltd
2014
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| Online Access: | http://hdl.handle.net/20.500.11937/16583 |
| _version_ | 1848749218407120896 |
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| author | Mahoney, S. Arfuso, Frank Millward, M. Dharmarajan, A. |
| author_facet | Mahoney, S. Arfuso, Frank Millward, M. Dharmarajan, A. |
| author_sort | Mahoney, S. |
| building | Curtin Institutional Repository |
| collection | Online Access |
| description | Background: Prostate cancer is associated with a poor survival rate. The ability of cancer cells to evade apoptosis and exhibit limitless replication potential allows for progression of cancer from a benign to a metastatic phenotype. The aim of this study was to investigate in vitro the effect of the isoflavone phenoxodiol on the expression of cell cycle genes. Methods: Three prostate cancer cell lines-LNCaP, DU145, and PC3 were cultured in vitro, and then treated with phenoxodiol (10 μM and 30 μM) for 24 and 48 h. The expression of cell cycle genes p21WAF1, c-Myc, Cyclin-D1, and Ki-67 was investigated by Real Time PCR. Results: Here we report that phenoxodiol induces cell cycle arrest in the G1/S phase of the cell cycle, with the resultant arrest due to the upregulation of p21WAF1 in all the cell lines in response to treatment, indicating that activation of p21WAF1 and subsequent cell arrest was occurring via a p53 independent manner, with induction of cytotoxicity independent of caspase activation. We found that c-Myc and Cyclin-D1 expression was not consistently altered across all cell lines but Ki-67 signalling expression was decreased in line with the cell cycle arrest. Conclusions: Phenoxodiol demonstrates an ability in prostate cancer cells to induce significant cytotoxicity in cells by interacting with p21WAF1 and inducing cell cycle arrest irrespective of p53 status or caspase pathway interactions. These data indicate that phenoxodiol would be effective as a potential future treatment modality for both hormone sensitive and hormone refractory prostate cancer. |
| first_indexed | 2025-11-14T07:17:27Z |
| format | Journal Article |
| id | curtin-20.500.11937-16583 |
| institution | Curtin University Malaysia |
| institution_category | Local University |
| last_indexed | 2025-11-14T07:17:27Z |
| publishDate | 2014 |
| publisher | BioMed Central Ltd |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | curtin-20.500.11937-165832017-09-13T15:44:33Z The effects of phenoxodiol on the cell cycle of prostate cancer cell lines Mahoney, S. Arfuso, Frank Millward, M. Dharmarajan, A. Cytotoxicity Prostate cancer Cell cycle Phenoxodiol Background: Prostate cancer is associated with a poor survival rate. The ability of cancer cells to evade apoptosis and exhibit limitless replication potential allows for progression of cancer from a benign to a metastatic phenotype. The aim of this study was to investigate in vitro the effect of the isoflavone phenoxodiol on the expression of cell cycle genes. Methods: Three prostate cancer cell lines-LNCaP, DU145, and PC3 were cultured in vitro, and then treated with phenoxodiol (10 μM and 30 μM) for 24 and 48 h. The expression of cell cycle genes p21WAF1, c-Myc, Cyclin-D1, and Ki-67 was investigated by Real Time PCR. Results: Here we report that phenoxodiol induces cell cycle arrest in the G1/S phase of the cell cycle, with the resultant arrest due to the upregulation of p21WAF1 in all the cell lines in response to treatment, indicating that activation of p21WAF1 and subsequent cell arrest was occurring via a p53 independent manner, with induction of cytotoxicity independent of caspase activation. We found that c-Myc and Cyclin-D1 expression was not consistently altered across all cell lines but Ki-67 signalling expression was decreased in line with the cell cycle arrest. Conclusions: Phenoxodiol demonstrates an ability in prostate cancer cells to induce significant cytotoxicity in cells by interacting with p21WAF1 and inducing cell cycle arrest irrespective of p53 status or caspase pathway interactions. These data indicate that phenoxodiol would be effective as a potential future treatment modality for both hormone sensitive and hormone refractory prostate cancer. 2014 Journal Article http://hdl.handle.net/20.500.11937/16583 10.1186/s12935-014-0110-z BioMed Central Ltd fulltext |
| spellingShingle | Cytotoxicity Prostate cancer Cell cycle Phenoxodiol Mahoney, S. Arfuso, Frank Millward, M. Dharmarajan, A. The effects of phenoxodiol on the cell cycle of prostate cancer cell lines |
| title | The effects of phenoxodiol on the cell cycle of prostate cancer cell lines |
| title_full | The effects of phenoxodiol on the cell cycle of prostate cancer cell lines |
| title_fullStr | The effects of phenoxodiol on the cell cycle of prostate cancer cell lines |
| title_full_unstemmed | The effects of phenoxodiol on the cell cycle of prostate cancer cell lines |
| title_short | The effects of phenoxodiol on the cell cycle of prostate cancer cell lines |
| title_sort | effects of phenoxodiol on the cell cycle of prostate cancer cell lines |
| topic | Cytotoxicity Prostate cancer Cell cycle Phenoxodiol |
| url | http://hdl.handle.net/20.500.11937/16583 |