The effect of Apigenin on glycometabolism and cell death in an anaplastic thyroid cancer cell line.
Anaplastic thyroid cancer
Apigenin
Apoptosis
Glucose transporter
Glucose uptake
Programmed cell death
Journal
Toxicology and applied pharmacology
ISSN: 1096-0333
Titre abrégé: Toxicol Appl Pharmacol
Pays: United States
ID NLM: 0416575
Informations de publication
Date de publication:
15 09 2023
15 09 2023
Historique:
received:
11
06
2023
revised:
02
07
2023
accepted:
05
07
2023
medline:
28
8
2023
pubmed:
13
7
2023
entrez:
12
7
2023
Statut:
ppublish
Résumé
A more pronounced characteristic of cancer cells is the energy dependence on glucose, which mitigated by glucose transporters. The comprehension of the regulatory mechanisms behind the Warburg effect holds promise for developing therapeutic interventions for cancers. Studies are lacking which targeted the GLUTs for treatment of malignancy of thyroid tumors. In our current investigation, we have undertaken this study to determine the potential of Apigenin, plant derived flavonoid in modulating tumor apoptosis by targeting GLUTs expression in SW1736 cell line of anaplastic thyroid carcinoma. Flow cytometry with propidium iodide staining was used to determine cell apoptosis. For glucose uptake detection, the "GOD-PAP" enzymatic colorimetric test was used to measure the direct glucose levels inside the cells. To determine the expression of GLUT1 and GLUT3 mRNA in the SW1736 cell line qRT-PCR was employed. Protein levels of GLUT1 and GLUT3 in the SW1736 cell line were detected with western blotting. Also, the scratch wound healing assay was conducted for cell migration. According to qRT-PCR analysis, the levels of GLUT1 and GLUT3 mRNA were lower in the group that received Apigenin relative to the control group. The Apigenin treatment of SW1736 cells decreased protein expression of the GLUT1 and GLUT3 levels in conformity to qRT-PCR. The scratch assays revealed that Apigenin treatment of cancer cell lines inhibited cell migration as compared to control. These findings demonstrate the possibility of targeting the glucose facilitators' pathway for making thyroid cancer cells more susceptible to programmed cell death.
Sections du résumé
AIMS AND BACKGROUND
A more pronounced characteristic of cancer cells is the energy dependence on glucose, which mitigated by glucose transporters. The comprehension of the regulatory mechanisms behind the Warburg effect holds promise for developing therapeutic interventions for cancers. Studies are lacking which targeted the GLUTs for treatment of malignancy of thyroid tumors. In our current investigation, we have undertaken this study to determine the potential of Apigenin, plant derived flavonoid in modulating tumor apoptosis by targeting GLUTs expression in SW1736 cell line of anaplastic thyroid carcinoma.
MATERIAL METHODS
Flow cytometry with propidium iodide staining was used to determine cell apoptosis. For glucose uptake detection, the "GOD-PAP" enzymatic colorimetric test was used to measure the direct glucose levels inside the cells. To determine the expression of GLUT1 and GLUT3 mRNA in the SW1736 cell line qRT-PCR was employed. Protein levels of GLUT1 and GLUT3 in the SW1736 cell line were detected with western blotting. Also, the scratch wound healing assay was conducted for cell migration.
RESULTS
According to qRT-PCR analysis, the levels of GLUT1 and GLUT3 mRNA were lower in the group that received Apigenin relative to the control group. The Apigenin treatment of SW1736 cells decreased protein expression of the GLUT1 and GLUT3 levels in conformity to qRT-PCR. The scratch assays revealed that Apigenin treatment of cancer cell lines inhibited cell migration as compared to control.
CONCLUSION
These findings demonstrate the possibility of targeting the glucose facilitators' pathway for making thyroid cancer cells more susceptible to programmed cell death.
Identifiants
pubmed: 37437745
pii: S0041-008X(23)00265-X
doi: 10.1016/j.taap.2023.116626
pii:
doi:
Substances chimiques
Apigenin
7V515PI7F6
Glucose Transporter Type 1
0
Glucose Transporter Type 3
0
Glucose
IY9XDZ35W2
RNA, Messenger
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
116626Informations de copyright
Copyright © 2023. Published by Elsevier Inc.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no competing interests.