TY  - JOUR
A1  - Makarević, Jasmina
A1  - Rutz, Jochen
A1  - Jüngel, Eva
A1  - Kaulfuß, Silke
A1  - Reiter, Michael Andreas
A1  - Tsaur, Igor
A1  - Bartsch, Georg
A1  - Haferkamp, Axel
A1  - Blaheta, Roman A.
T1  - Amygdalin blocks bladder cancer cell growth in vitro by diminishing cyclin A and cdk2
T2  - PLoS One
N2  - Amygdalin, a natural compound, has been used by many cancer patients as an alternative approach to treat their illness. However, whether or not this substance truly exerts an anti-tumor effect has never been settled. An in vitro study was initiated to investigate the influence of amygdalin (1.25–10 mg/ml) on the growth of a panel of bladder cancer cell lines (UMUC-3, RT112 and TCCSUP). Tumor growth, proliferation, clonal growth and cell cycle progression were investigated. The cell cycle regulating proteins cdk1, cdk2, cdk4, cyclin A, cyclin B, cyclin D1, p19, p27 as well as the mammalian target of rapamycin (mTOR) related signals phosphoAkt, phosphoRaptor and phosphoRictor were examined. Amygdalin dose-dependently reduced growth and proliferation in all three bladder cancer cell lines, reflected in a significant delay in cell cycle progression and G0/G1 arrest. Molecular evaluation revealed diminished phosphoAkt, phosphoRictor and loss of Cdk and cyclin components. Since the most outstanding effects of amygdalin were observed on the cdk2-cyclin A axis, siRNA knock down studies were carried out, revealing a positive correlation between cdk2/cyclin A expression level and tumor growth. Amygdalin, therefore, may block tumor growth by down-modulating cdk2 and cyclin A. In vivo investigation must follow to assess amygdalin's practical value as an anti-tumor drug.
Y1  - 2014
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/35035
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-350359
SN  - 1932-6203
N1  - Copyright: © 2014 Makarevic et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
VL  - 9
IS  - (8):e105590
PB  - PLoS
CY  - Lawrence, Kan.
ER  -