skip to main content

Twist2 contributes to breast cancer progression by promoting an epithelial–mesenchymal transition and cancer stem-like cell self-renewal

X Fang ; Y Cai ; J Liu ; Z Wang ; Q Wu ; Z Zhang ; C J Yang ; L Yuan ; G Ouyang

Oncogene, 2011, Vol.30(47), p.4707 [Periódico revisado por pares]

Texto completo disponível

Citações Citado por
  • Título:
    Twist2 contributes to breast cancer progression by promoting an epithelial–mesenchymal transition and cancer stem-like cell self-renewal
  • Autor: X Fang ; Y Cai ; J Liu ; Z Wang ; Q Wu ; Z Zhang ; C J Yang ; L Yuan ; G Ouyang
  • Assuntos: Breast Cancer -- Risk Factors ; Breast Cancer -- Genetic Aspects ; Breast Cancer -- Development And Progression ; Breast Cancer -- Research ; Cellular Signal Transduction -- Genetic Aspects ; Cellular Signal Transduction -- Health Aspects ; Cellular Signal Transduction -- Research ; Transcription Factors -- Physiological Aspects ; Transcription Factors -- Research
  • É parte de: Oncogene, 2011, Vol.30(47), p.4707
  • Descrição: The epithelial to mesenchymal transition (EMT) is a highly conserved cellular programme that has an important role in normal embryogenesis and in cancer invasion and metastasis. We report here that Twist2, a tissue-specific basic helix-loop-helix transcription factor, is overexpressed in human breast cancers and lymph node metastases. In mammary epithelial cells and breast cancer cells, ectopic overexpression of Twist2 results in morphological transformation, downregulation of epithelial markers and upregulation of mesenchymal markers. Moreover, Twist2 enhances the cell migration and colony-forming abilities of mammary epithelial cells and breast cancer cells in vitro and promotes tumour growth in vivo. Ectopic expression of Twist2 in mammary epithelial cells and breast cancer cells increases the size and number of their [CD44.sup.high]/[CD24.sup.low] stem-like cell sub-populations, promotes the expression of stem cell markers and enhances the self-renewal capabilities of stem-like cells. In addition, exogenous expression of Twist2 leads to constitutive activation of STAT3 (signal transducer and activator of transcription 3) and downregulation of E-cadherin. Thus, the overexpression of Twist2 may contribute to breast cancer progression by activating the EMT programme and enhancing the self-renewal of cancer stem-like cells. Oncogene (2011) 30, 4707-1720; doi: 10.1038/onc.2011.181; published online 23 May 2011 Keywords: Twist2; epithelial-mesenchymal transition; cancer stem cell; breast cancer; metastasis

Buscando em bases de dados remotas. Favor aguardar.