Inhibition of NF-kB/IL-6/JAK2/STAT3 Pathway and Epithelial-Mesenchymal Transition in Breast Cancer Cells by Azilsartan.
Humans
Female
Epithelial-Mesenchymal Transition
NF-kappa B
/ metabolism
Interleukin-6
/ metabolism
Matrix Metalloproteinase 9
/ metabolism
Breast Neoplasms
/ drug therapy
bcl-2-Associated X Protein
/ metabolism
Cell Line, Tumor
RNA, Messenger
Janus Kinase 2
/ metabolism
STAT3 Transcription Factor
/ genetics
EMT
IL-6/JAK2/STAT3
NF-kB
SLUG
SNAIL
TWIST
azilsartan
breast cancer
Journal
Molecules (Basel, Switzerland)
ISSN: 1420-3049
Titre abrégé: Molecules
Pays: Switzerland
ID NLM: 100964009
Informations de publication
Date de publication:
13 Nov 2022
13 Nov 2022
Historique:
received:
30
09
2022
revised:
09
11
2022
accepted:
10
11
2022
entrez:
26
11
2022
pubmed:
27
11
2022
medline:
30
11
2022
Statut:
epublish
Résumé
Metastatic breast cancer is an incurable form of breast cancer that exhibits high levels of epithelial-mesenchymal transition (EMT) markers. Angiotensin II has been linked to various signaling pathways involved in tumor cell growth and metastasis. The aim of this study is to investigate, for the first time, the anti-proliferative activity of azilsartan, an angiotensin II receptor blocker, against breast cancer cell lines MCF-7 and MDA-MB-231 at the molecular level. Cell viability, cell cycle, apoptosis, colony formation, and cell migration assays were performed. RT-PCR and western blotting analysis were used to explain the molecular mechanism. Azilsartan significantly decreased the cancer cells survival, induced apoptosis and cell cycle arrest, and inhibited colony formation and cell migration abilities. Furthermore, azilsartan reduced the mRNA levels of
Identifiants
pubmed: 36431925
pii: molecules27227825
doi: 10.3390/molecules27227825
pmc: PMC9693603
pii:
doi:
Substances chimiques
NF-kappa B
0
azilsartan
F9NUX55P23
Interleukin-6
0
Matrix Metalloproteinase 9
EC 3.4.24.35
bcl-2-Associated X Protein
0
RNA, Messenger
0
JAK2 protein, human
EC 2.7.10.2
Janus Kinase 2
EC 2.7.10.2
STAT3 protein, human
0
STAT3 Transcription Factor
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : JSPS KAKENHI Grant Number (JP21K07614)
ID : (JP21K07614)
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