Rotundic acid induces Cas3-MCF-7 cell apoptosis through the p53 pathway.

Abstract:

:In the present study, the functions and mechanisms of rotundic acid (RA) underlying its induction of apoptosis in caspase-3-transfected MCF-7 human breast cancer cells (Cas3-MCF-7 cells) were investigated. RA induced apoptosis in Cas3-MCF-7 cells more efficiently compared with that in MCF-7 cells transfected with control plasmid. The results from an MTT assay demonstrated that RA effectively inhibited Cas3-MCF-7 cell viability in a dose-dependent manner and induced cell apoptosis via caspase-3 activity within 12 to 48 h. Western blotting and fluorescence-activated cell sorting demonstrated that RA initiated Cas3-MCF-7 cell apoptosis via p53 activation. The silencing of the p53 gene in the Cas3-MCF-7 cell line led to decreased RA-induced Cas3-MCF-7 cell caspase-3 activity and cell apoptosis. Collectively, the results of the present study indicate that caspase-3 serves a critical function in rotundic acid-induced apoptosis, and suggest that caspase-3 deficiency may contribute to the chemotherapy-resistance of breast cancer. Reconstitution of caspase-3 sensitizes MCF-7 breast cancer cells to chemotherapy. RA has the potential for development as a novel drug combined with reconstitution of caspase-3 gene therapy for the treatment of human breast cancer with caspase-3 deficiency.

journal_name

Oncol Lett

journal_title

Oncology letters

authors

Nan ML,Wang X,Li HJ,Yu DH,Sun WY,Xu HM,He YF,Zhao QC

doi

10.3892/ol.2018.9616

subject

Has Abstract

pub_date

2019-01-01 00:00:00

pages

630-637

issue

1

eissn

1792-1074

issn

1792-1082

pii

OL-0-0-9616

journal_volume

17

pub_type

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