Fe3O4-solamargine induces apoptosis and inhibits metastasis of pancreatic cancer cells.
Animals
Antineoplastic Agents, Phytogenic
/ chemistry
Apoptosis
/ drug effects
Biomarkers, Tumor
/ genetics
Cell Cycle Checkpoints
/ drug effects
Cell Line, Tumor
Cell Movement
/ drug effects
Cell Survival
/ drug effects
Drug Delivery Systems
Ferrosoferric Oxide
/ chemistry
Gene Expression Regulation, Neoplastic
/ drug effects
Humans
Liposomes
/ chemistry
Male
Mice
Neoplasm Invasiveness
Pancreatic Neoplasms
/ metabolism
Signal Transduction
/ drug effects
Solanaceous Alkaloids
/ chemistry
Xenograft Model Antitumor Assays
solamargine
Fe3O4-solamargine
magnetic resonance imaging
pancreatic cancer
Journal
International journal of oncology
ISSN: 1791-2423
Titre abrégé: Int J Oncol
Pays: Greece
ID NLM: 9306042
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
24
04
2018
accepted:
30
07
2018
pubmed:
30
11
2018
medline:
21
5
2019
entrez:
29
11
2018
Statut:
ppublish
Résumé
Fe3O4-magnetic liposome (MLP) can deliver drugs to target tissues and can increase drug efficacy. The present study aimed to investigate the effects of solamargine (SM) and Fe3O4-SM in pancreatic cancer (PC). Cell viability was detected using a Cell Counting kit‑8 assay. Apoptosis and cell cycle progression was tested using a flow cytometry assay. A scratch assay was used to examine cell metastasis. Quantitative polymerase chain reaction, western blot analysis or immunohistochemical analysis were performed to determine the expression of target factors. Magnetic resonance imagining (MRI) and terminal deoxynucleotidyl-transferase-mediated dUTP nick end labelling were conducted to detect tumor growth and apoptosis in vivo, respectively. It was demonstrated that Fe3O4-SM inhibited cancer cell growth via a slow release of SM over an extended period of time. SM was revealed to induce apoptosis and cell cycle arrest. Furthermore, SM decreased the expression of X-linked inhibitor of apoptosis, Survivin, Ki‑67, proliferating cell nuclear antigen and cyclin D1, but increased the activity of caspase-3. It was also observed that SM inhibited tumor cell metastasis by modulating the expression of matrix metalloproteinase (MMP)-2 and TIMP metallopeptidase inhibitor-2. Furthermore, the phosphorylation of protein kinase B and mechanistic target of rapamycin was suppressed by SM. Notably, the effect of SM was enhanced by Fe3O4-SM. The malignant growth of PC was decreased by SM in vivo. Furthermore, the expression of Ki‑67 was decreased by SM and Fe3O4-SM. Additionally, cell apoptosis was increased in the Fe3O4-SM group, compared with the SM group. The present study illustrated the antitumor effect and action mec-hanism produced by SM. Additionally, it was demonstrated that Fe3O4-SM was more effective than SM in protecting against PC.
Identifiants
pubmed: 30483763
doi: 10.3892/ijo.2018.4637
pmc: PMC6365027
doi:
Substances chimiques
Antineoplastic Agents, Phytogenic
0
Biomarkers, Tumor
0
Liposomes
0
Solanaceous Alkaloids
0
beta-solamarine
3671-38-3
Ferrosoferric Oxide
XM0M87F357
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
905-915Références
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