Regulation of Differentiation of HC11 Mouse Breast Epithelial Cells by the Signal Transducer and Activator of Transcription-3.
E-cadherin
Stat3
cell differentiation
Journal
Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988
Informations de publication
Date de publication:
Jun 2019
Jun 2019
Historique:
received:
11
03
2019
revised:
24
04
2019
accepted:
03
05
2019
entrez:
10
6
2019
pubmed:
10
6
2019
medline:
18
6
2019
Statut:
ppublish
Résumé
The differentiation of the mouse breast epithelial cell line HC11 is known to require confluence as well as the addition of hydrocortisone, insulin and prolactin. Since confluence, which triggers the engagement of the cell-to-cell adhesion molecule E-cadherin, induces a dramatic increase in the activity of signal transducer and activator of transcription-3 (Stat3), we examined the role of Stat3 in HC11 cell differentiation. Stat3 inhibition abolished differentiation, indicating that Stat3 activity is critically required. However, expression of the mutationally activated form of Stat3 (Stat3C), rather than promoting, it was found to block cell differentiation, even when expressed in low levels, and in the absence of full neoplastic conversion. The strength of the E-cadherin/Stat3 signal is key for the outcome of the differentiation process.
Sections du résumé
BACKGROUND/AIM
OBJECTIVE
The differentiation of the mouse breast epithelial cell line HC11 is known to require confluence as well as the addition of hydrocortisone, insulin and prolactin.
MATERIALS AND METHODS
METHODS
Since confluence, which triggers the engagement of the cell-to-cell adhesion molecule E-cadherin, induces a dramatic increase in the activity of signal transducer and activator of transcription-3 (Stat3), we examined the role of Stat3 in HC11 cell differentiation.
RESULTS
RESULTS
Stat3 inhibition abolished differentiation, indicating that Stat3 activity is critically required. However, expression of the mutationally activated form of Stat3 (Stat3C), rather than promoting, it was found to block cell differentiation, even when expressed in low levels, and in the absence of full neoplastic conversion.
CONCLUSION
CONCLUSIONS
The strength of the E-cadherin/Stat3 signal is key for the outcome of the differentiation process.
Identifiants
pubmed: 31177110
pii: 39/6/2749
doi: 10.21873/anticanres.13401
doi:
Substances chimiques
Cadherins
0
Cdh1 protein, mouse
0
STAT3 Transcription Factor
0
Stat3 protein, mouse
0
Tyrosine
42HK56048U
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2749-2756Informations de copyright
Copyright© 2019, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.