Oncostatic treatment effect of triple negative breast cancer cell line with copper (I)-nicotinate complex.
Antineoplastic Agents
/ chemistry
Antioxidants
/ chemistry
Apoptosis
/ drug effects
Caspase 3
/ metabolism
Cell Cycle Checkpoints
/ drug effects
Cell Line, Tumor
Cell Survival
/ drug effects
Checkpoint Kinase 1
/ metabolism
Copper
/ chemistry
Female
Gene Expression
Humans
Niacin
/ chemistry
Phosphorylation
/ drug effects
Programmed Cell Death 1 Receptor
Superoxide Dismutase
/ metabolism
Survivin
/ genetics
Triple Negative Breast Neoplasms
/ metabolism
apoptosis
caspase-3
copper (I)-nicotinate complex (CNC)
programmed cell death protein-1 (PD-1)
survivin
triple-negative breast cancer (TNBC)
Journal
Journal of cellular biochemistry
ISSN: 1097-4644
Titre abrégé: J Cell Biochem
Pays: United States
ID NLM: 8205768
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
08
02
2018
accepted:
29
08
2018
pubmed:
27
10
2018
medline:
9
4
2020
entrez:
27
10
2018
Statut:
ppublish
Résumé
The treatment of triple-negative breast cancer (TNBC) remains a major challenge. The present study aimed to throw more light on the role of copper (I)-nicotinate complex (CNC) as an antitumor as well as a proapoptotic agent. In this study, the HCC-1806 cell line was used as a model for TNBC. Cell cycle, apoptosis assay, and programmed cell death protein-1 were investigated by flowcytometry. Besides, the comet assay was performed using a fluorescence microscope. The enzyme-linked immunosorbent assay technique was used for the detection of phospho-Chk1 at ser 317 and caspase-3. Moreover, the gene expression of survivin was identified by real-time polymerase chain reaction. Finally, superoxide dismutase (SOD) was calorimetrically assayed. The viability of HCC-1806 cells treated with CNC was decreased in a dose-dependent manner. The tendency for apoptotic machinery was observed through the increase in the sub G0 peak, the percentage of early and late apoptotic phases, and the elevation in caspase-3 levels associated with a downregulation of the survivin gene expression. The antioxidant property of the complex, reflected by elevated SOD activity, may contribute to mediate the cell death pathways. Low concentrations of CNC were found to favor the apoptotis-mediated mechanism. However, one cannot neglect the abundance of cell necrosis-mediated death of cells via CNC, especially at higher concentrations.
Substances chimiques
Antineoplastic Agents
0
Antioxidants
0
PDCD1 protein, human
0
Programmed Cell Death 1 Receptor
0
Survivin
0
Niacin
2679MF687A
Copper
789U1901C5
Superoxide Dismutase
EC 1.15.1.1
CHEK1 protein, human
EC 2.7.11.1
Checkpoint Kinase 1
EC 2.7.11.1
CASP3 protein, human
EC 3.4.22.-
Caspase 3
EC 3.4.22.-
cupric chloride
S2QG84156O
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
4278-4290Informations de copyright
© 2018 Wiley Periodicals, Inc.