التفاصيل البيبلوغرافية
| العنوان: |
Loss of polarity alters proliferation and differentiation in low-grade endometrial cancers by disrupting Notch signaling. |
| المؤلفون: |
Williams, Erin1,2, Villar-Prados, Alejandro1,2, Bowser, Jessica3, Broaddus, Russell2,4, Gladden, Andrew B.1,2 agladden@mdanderson.org |
| المصدر: |
PLoS ONE. 12/05/2017, Vol. 12 Issue 12, p1-20. 20p. |
| مصطلحات موضوعية: |
*CELL adhesion, *EPITHELIUM, *HOMEOSTASIS, *ENDOMETRIAL cancer, *NOTCH signaling pathway, *ANATOMY |
| مستخلص: |
Cell adhesion and apicobasal polarity together maintain epithelial tissue organization and homeostasis. Loss of adhesion has been described as a prerequisite for the epithelial to mesenchymal transition. However, what role misregulation of apicobasal polarity promotes tumor initiation and/or early progression remains unclear. We find that human low-grade endometrial cancers are associated with disrupted localization of the apical polarity protein Par3 and Ezrin while, the adhesion molecule E-cadherin remains unchanged, accompanied by decreased Notch signaling, and altered Notch receptor localization. Depletion of Par3 or Ezrin, in a cell-based model, results in loss of epithelial architecture, differentiation, increased proliferation, migration and decreased Notch signaling. Re-expression of Par3 in endometrial cancer cell lines with disrupted Par3 protein levels blocks proliferation and reduces migration in a Notch dependent manner. These data uncover a function for apicobasal polarity independent of cell adhesion in regulating Notch-mediated differentiation signals in endometrial epithelial cells. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
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