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

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

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.

MeSH terms

  • Animals
  • Cadherins / metabolism
  • Cell Differentiation
  • Epithelial Cells / cytology*
  • Female
  • Mammary Glands, Animal / cytology*
  • Mammary Glands, Animal / metabolism
  • Mice
  • Mutation
  • Phosphorylation
  • STAT3 Transcription Factor / genetics*
  • STAT3 Transcription Factor / metabolism*
  • Signal Transduction
  • Tyrosine / metabolism

Substances

  • Cadherins
  • Cdh1 protein, mouse
  • STAT3 Transcription Factor
  • Stat3 protein, mouse
  • Tyrosine