Treating MCF7 breast cancer cell with proteasome inhibitor Bortezomib restores apoptotic factors and sensitizes cell to Docetaxel.
Adenosine Triphosphate
/ metabolism
Antineoplastic Combined Chemotherapy Protocols
/ pharmacology
Apoptosis
/ drug effects
Apoptotic Protease-Activating Factor 1
/ genetics
Bortezomib
/ administration & dosage
Caspase 3
/ metabolism
Caspase 7
/ metabolism
Cell Movement
/ drug effects
Cell Survival
/ drug effects
DNA Fragmentation
/ drug effects
Docetaxel
/ administration & dosage
Enzyme Activation
/ drug effects
Humans
MCF-7 Cells
Proteasome Inhibitors
/ administration & dosage
Reactive Oxygen Species
/ metabolism
Apaf-1
Apoptosis induction
Bortezomib
Docetaxel
Proteasome inhibitor
Journal
Medical oncology (Northwood, London, England)
ISSN: 1559-131X
Titre abrégé: Med Oncol
Pays: United States
ID NLM: 9435512
Informations de publication
Date de publication:
27 Apr 2021
27 Apr 2021
Historique:
received:
03
03
2021
accepted:
05
04
2021
entrez:
27
4
2021
pubmed:
28
4
2021
medline:
30
11
2021
Statut:
epublish
Résumé
Chemoresistance is the leading cause of limiting long-term treatment success in cancer cells. Anticancer drugs usually kill cells through apoptosis induction and defects in this signaling pathway lead to chemoresistance. Apoptotic protease activating factor 1 regulates cellular stress evoked by chemotherapeutic agents through facilitating apoptosome assembling but can be degraded by proteasome. This study examined the role of proteasome inhibitor Bortezomib in the cytotoxic effects of Docetaxel on MCF7 cells response and its correlation with Apaf-1 expression level. MTT assay, caspase 3/7 activity assay, propidium iodide staining, adenosine triphosphate and reactive oxygen species amount measurements were utilized to demonstrate the role of Bortezomib in Docetaxel efficacy with and without Apaf-1 overexpressing. Meanwhile, two-dimensional cell migration assay was performed by scratch wound assay. The combination of Docetaxel with Bortezomib was significantly more cytotoxic compared single drug, more effectively delayed cell growth, reduced ATP level and increased ROS production. In Apaf-1 overexpressing, Docetaxel was more efficient in preventing cell migration, however, Docetaxel plus Bortezomib were not significantly effective; and fluorescence images supported the interpretation. Our findings demonstrated MCF7 resistance to Docetaxel is due in part to low Apaf-1 level and Apaf-1 overexpression resulted in the increase of cell susceptibility to Docetaxel stimulus. We assume that proteasome inhibitor may restore apoptotic proteins like Apaf-1 and prevent the degradation of cytosolic cytochrome c released by Docetaxel, consequently triggering intrinsic apoptosis and promoting cancer cell death. Collectively, treating MCF7 breast cells with proteasome inhibitor sensitizes cells to Docetaxel-induced apoptosis and possibly overcomes chemoresistance.
Identifiants
pubmed: 33904968
doi: 10.1007/s12032-021-01509-7
pii: 10.1007/s12032-021-01509-7
doi:
Substances chimiques
APAF1 protein, human
0
Apoptotic Protease-Activating Factor 1
0
Proteasome Inhibitors
0
Reactive Oxygen Species
0
Docetaxel
15H5577CQD
Bortezomib
69G8BD63PP
Adenosine Triphosphate
8L70Q75FXE
CASP3 protein, human
EC 3.4.22.-
CASP7 protein, human
EC 3.4.22.-
Caspase 3
EC 3.4.22.-
Caspase 7
EC 3.4.22.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
64Références
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