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Experimental cell research v.361 no.1, 2017년, pp.112 - 125   SCI SCIE
본 등재정보는 저널의 등재정보를 참고하여 보여주는 베타서비스로 정확한 논문의 등재여부는 등재기관에 확인하시기 바랍니다.

Regulation of HC11 mouse breast epithelial cell differentiation by the E-cadherin/Rac axis

Niit, Maximilian    (Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada K7L 3N6   ); Arulanandam, Rozanne    (Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada K7L 3N6   ); Cass, Jamaica    (Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada K7L 3N6   ); Geletu, Mulu    (Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada K7L 3N6   ); Hoskin, Victoria    (Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada K7L3N6   ); Côté, Graham    (Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada K7L 3N6   ); Gunning, Patrick    (Department of Chemical and Physical Sciences, University of Toronto, Mississauga, Ontario, Canada L5L 1C6   ); Elliott, Bruce    (Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada K7L3N6   ); Raptis, Leda    (Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada K7L 3N6  );

  • 초록  

    Abstract It was previously demonstrated that differentiation of some established breast epithelial cell lines requires confluence and stimulation with hydrocortisone, insulin and prolactin inducers. We and others previously demonstrated that E-cadherin engagement, which is favored under conditions of confluence, increases the levels and activity of the Rac small GTPase. To investigate the functional relationship between the transforming ability of Rac and its role as an integral component of the differentiative E-cadherin signaling pathway, we introduced a mutationally activated form of Rac, Rac V12 , into the mouse breast epithelium-derived cell line, HC11. Our results demonstrate that the strength of the Rac signal is key for the outcome of the differentiation process; cRac1 is critically required for differentiation, and at low levels, mutationally activated Rac V12 is able to in crease differentiation, presumably reinforcing the E-cadherin/Rac differentiative signal. However, high Rac V12 expression blocked differentiation concomitant with E-cadherin downregulation, while inducing neoplastic transformation. Therefore, the intensity of the Rac signal is a central determinant in the balance between cell proliferation vs differentiation, two fundamentally opposed processes, a finding which could also have important therapeutic implications.


  • 주제어

    E-cadherin .   Rac .   Mammary epithelial cells .   Differentiation .   Stat3.  

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