β-elemene induced anticancer effect in bladder cancer through upregulation of PTEN and suppression of AKT phosphorylation
Human bladder cancer is one of the most aggressive tumours known and has shown resistance to traditional chemotherapy, which depends heavily on DNA-damaging drugs. β-elemene is one of the least cytotoxic antitumor agents that are extracted from Curcuma aromatica salisb and it exhibits antitumor effe...
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Veröffentlicht in: | Oncology letters 2018-11, Vol.16 (5), p.6019-6025 |
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Sprache: | eng |
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Zusammenfassung: | Human bladder cancer is one of the most aggressive tumours known and has shown resistance to traditional chemotherapy, which depends heavily on DNA-damaging drugs. β-elemene is one of the least cytotoxic antitumor agents that are extracted from Curcuma aromatica salisb and it exhibits antitumor effects in many carcinomas. β-elemene has attracted the attention of clinicians and scientists worldwide due to its few side effects and limited effect on the bone marrow. However, the antitumor mechanism of β-elemene remains largely unstudied. In the present study, the expression of the AKT serine/threonine kinase (AKT) signaling pathway in bladder cancer and normal bladder tissue was investigated, and the influence of β-elemene on bladder cancer cells and the mechanisms involved were assessed. The results showed that phosphatase and tensin homolog deleted on chromosome ten (PTEN) was downregulated and phosphorylated-AKT (pAKT) was overexpressed in human bladder cancer. β-elemene significantly suppressed the viability of bladder cancer cells, while leaving normal bladder cells unaffected. In addition, there was an increased number of apoptotic bladder cancer cells following β-elemene treatment, and a significant reduction in cell invasion and migration. Subsequent western blot analyses revealed that bladder cancer cells treated with β-elemene had increased PTEN expression and decreased expression of pAKT. Taken together, these results suggest that β-elemene has an antitumor effect in bladder cancer cells through the upregulation of PTEN and suppression of AKT phosphorylation. |
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ISSN: | 1792-1074 1792-1082 |
DOI: | 10.3892/ol.2018.9401 |