Exploring the Potential Mechanism of Costunolide‐Induced MCF‐7 Cells Apoptosis by Multi‐Spectroscopy, Molecular Docking and Cell Experiments

Exploring the Potential Mechanism of Costunolide‐Induced MCF‐7 Cells Apoptosis by Multi‐Spectroscopy, Molecular Docking and Cell Experiments

Breast cancer is one of the most common cancer with high morbidity and mortality in women. This study aimed to explore the potential mechanism of costunolide inducing MCF‐7 cells apoptosis by multi‐spectroscopy, molecular docking, and cell experiments. The results manifested that costunolide interac...

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Bibliographic Details
Published in:Chemistry & biodiversity Vol. 18; no. 5; pp. e2001069 - n/a
Main Authors: Liu, Dan, Zeng, Meng, Pi, Jing‐Wen, Liu, Mei‐Jia, Ding, Wei‐Zhe, Mei, Xue‐Ying, Liu, Jian‐Li, Cao, Xiang‐Yu
Format: Journal Article
Language:English
Published: Switzerland Wiley Subscription Services, Inc 01-05-2021
Subjects:
Apoptosis
Bax protein
Breast cancer
breast cancer MCF-7 cells
Calf thymus
calf thymus DNA
Caspase
Cell proliferation
costunolide
Deoxyribonucleic acid
DNA
DNA damage
Grooves
Molecular docking
Morbidity
p53 Protein
Spectroscopy
Spectrum analysis
calf thymus DNA
apoptosis
molecular docking
costunolide
breast cancer MCF-7 cells
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Summary:Breast cancer is one of the most common cancer with high morbidity and mortality in women. This study aimed to explore the potential mechanism of costunolide inducing MCF‐7 cells apoptosis by multi‐spectroscopy, molecular docking, and cell experiments. The results manifested that costunolide interacted with calf thymus DNA (ct‐DNA) in a spontaneous manner, and the minor groove as the preferential binding mode. Furthermore, costunolide inhibited cell proliferation and colony formation. Hoechst 33258 staining showed that cell apoptosis induced by costunolide might be related to DNA damage. The apoptosis mechanism relied on regulating the protein expression of Bax, Bcl‐2, p53, Caspase‐3 and the activation of p38MAPK and nuclear factor κB (NF‐κB) pathways. This study will provide some experimental basis and potential therapeutic strategy for breast cancer treatment.
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ISSN:1612-1872
1612-1880
DOI:10.1002/cbdv.202001069