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Anticancer Res. 2019 Jun;39(6):2749-2756. doi: 10.21873/anticanres.13401.

Regulation of Differentiation of HC11 Mouse Breast Epithelial Cells by the Signal Transducer and Activator of Transcription-3.

Author information

1
Department of Biomedical and Molecular Sciences and Department of Pathology and Molecular Medicine, Queen's University, Kingston, ON, Canada.
2
Department of Chemical and Physical Sciences, University of Toronto, Mississauga, ON, Canada mulu.geletu@utoronto.ca.
3
Center for Innovative Cancer Research, Ottawa Hospital Research Institute, Ottawa, ON, Canada.

Abstract

BACKGROUND/AIM:

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:

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:

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:

The strength of the E-cadherin/Stat3 signal is key for the outcome of the differentiation process.

KEYWORDS:

E-cadherin; Stat3; cell differentiation

PMID:
31177110
DOI:
10.21873/anticanres.13401
[Indexed for MEDLINE]

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