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Slug and Sox9 Cooperatively Regulate Tumor Initiating Niche Factors in Breast Cancer Publisher



Fazilaty H1, 2, 5 ; Gardaneh M3 ; Akbari P3 ; Zekri A2 ; Behnam B1, 4
Authors
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Authors Affiliations
  1. 1. Cellular and Molecular Research Center (CMRC), Faculty of Medicine, Iran University of Medical Sciences (IUMS), Tehran, Iran
  2. 2. Department of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences (TUMS), Tehran, Iran
  3. 3. Department of Stem Cell, Institute of Medical Biotechnology, National Institute of Genetic Engineering and Biotechnology (NIGEB), Tehran, Iran
  4. 4. Department of Medical Genetics and Molecular Biology, Iran University of Medical Sciences (IUMS), Tehran, Iran
  5. 5. Instituto de Nuerociencias de Alicante (CSIC-UMH), San Juan de Alicante, Spain

Source: Cancer Microenvironment Published:2016


Abstract

Presence of tumor initiating cells and a proper niche is essential for metastatic colonization. SLUG and SOX9 transcription factors play essential roles in induction and maintenance of tumor initiating capacity in breast cancer cells. On the other hand, Tenascin-C and Periostin are crucial factors in metastatic niche that support tumor initiating capability in breast cancer. In this study, regulatory effect of SLUG and SOX9 transcription factors on the expression of Tenascin-C and Periostin was examined. SLUG and SOX9 were overexpressed and knocked-down in MCF7 and MDA-MB-231 cells, respectively. The cells as little and highly invasive breast cancer-derived cells were infected by inducing and shRNA lentivirus constructs. Then, Tenascin-C and Periostin as well as SLUG and SOX9 expression levels were measured in the cells via Real-Time PCR. Simultaneous overexpression of SLUG and SOX9 significantly induced Tenascin-C and Periostin expression. SLUG and SOX9 knock-down also significantly reduced the expression of Tenascin-C and Periostin. In this analysis Periostin showed the most deviation in both up- and down-regulation levels. This regulatory effect might shed light to a crosstalk between factors involved in the tumor initiating capacity and metastatic niche of the breast cancer. © 2015, Springer Science+Business Media Dordrecht.