Background: Recently, cytotoxic effects of statins on breast
cancer cells have been reported. However, the mechanism of antiproliferative
effects is currently unknown. Autophagy is non-apoptotic
programmed cell death, which is characterized by degradation of
cytoplasmic components and as having a role in cancer pathogenesis.
Aims: To investigate the anti-proliferative effects of atorvastatin
on MCF-7 human breast adenocarcinoma cells with respect to both
autophagy and apoptosis.
Study Design: Cell culture study.
Methods: Cell viability was analyzed using WST-1 cell proliferation
assay. Apoptosis was determined by the TUNEL method, whereas
autophagy was assessed by Beclin-1 and LC3B immunofluorescence
staining. Ultrastructural analysis of cells was performed by electron
microscopy.
Results: Atorvastatin reduced MCF-7 cell proliferation in a dose- and
time-dependent manner inducing TUNEL-, Beclin-1-, and LC3Bpositive
cells. Moreover, ultrastructural analysis showed apoptotic,
autophagic, and necrotic morphological changes in treatment groups.
A statistically significant increase in the apoptotic index was detected
with higher concentrations of atorvastatin at 24 h and 48 h (p<0.05).
Conclusion: The anti-proliferative effects of atorvastatin on breast
cancer cells is mediated by the induction of both apoptosis and
autophagy which shows statins as a potential treatment option for
breast cancer.
Apoptosis atorvastatin autophagy breast cancer cytotoxicity MCF-7 cells
Diğer ID | JA36GA37MH |
---|---|
Bölüm | Araştırma Makalesi |
Yazarlar | |
Yayımlanma Tarihi | 1 Mayıs 2018 |
Yayımlandığı Sayı | Yıl 2018 Cilt: 35 Sayı: 3 |