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Icaritin acts synergistically with epirubicin to suppress bladder cancer growth through inhibition of autophagy.
- Source :
-
Oncology reports [Oncol Rep] 2016 Jan; Vol. 35 (1), pp. 334-42. Date of Electronic Publication: 2015 Oct 16. - Publication Year :
- 2016
-
Abstract
- Bladder cancer is one of the most commonly diagnosed urological malignancies. Acquired resistance to chemotherapy is a great barrier for achieving successful treatment of bladder cancer. In the present study, we investigated the effect and mechanisms of icaritin, a flavonol glycoside derived from genus Epimedium, against human bladder cancer cells. It was found that despite the low cytotoxicity in normal human HEK293 cells, icaritin significantly inhibited the proliferation and colony formation of BT5637 and T24 bladder cancer cells time- and dose-dependently compared to the DMSO vehicle control. Moreover, cell viability monitored through mitochondrial membrane potential was inhibited markedly after icaritin treatment. Further investigation indicated that icaritin may inhibit epirubicin (EPI)-induced autophagy, and acted synergistically with EPI to suppress the proliferation of BT5637 and T24 cells. These findings suggest that icaritin may prove to be a novel potent therapeutic agent for the treatment of bladder cancer.
- Subjects :
- Cell Line, Tumor
Cell Proliferation drug effects
Cell Survival drug effects
Dose-Response Relationship, Drug
Drug Resistance, Neoplasm drug effects
Drug Synergism
HEK293 Cells
Humans
Membrane Potential, Mitochondrial drug effects
Time Factors
Urinary Bladder Neoplasms drug therapy
Autophagy drug effects
Epirubicin pharmacology
Flavonoids pharmacology
Urinary Bladder Neoplasms metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1791-2431
- Volume :
- 35
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Oncology reports
- Publication Type :
- Academic Journal
- Accession number :
- 26496799
- Full Text :
- https://doi.org/10.3892/or.2015.4335