Special AT-rich sequence-binding protein-1 participates in the maintenance of breast cancer stem cells through regulation of the Notch signaling pathway and expression of Snail1 and Twist1

Sun,Zhengkui; Zhang,Chao; Zou,Xuesen; Jiang,Guixiang; Xu,Zongquan; Li,Wenting; Xie,Hui

doi:10.3892/mmr.2015.3192

Special AT-rich sequence-binding protein-1 participates in the maintenance of breast cancer stem cells through regulation of the Notch signaling pathway and expression of Snail1 and Twist1

Authors:
- Zhengkui Sun
- Chao Zhang
- Xuesen Zou
- Guixiang Jiang
- Zongquan Xu
- Wenting Li
- Hui Xie
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Affiliations: Department of Breast Surgery, Jiangxi Cancer Hospital, Nanchang, Jiangxi 330029, P.R. China, Department of Clinical Medicine, Medical School of Nanchang University, Nanchang, Jiangxi 330029, P.R. China
Published online on: January 13, 2015 https://doi.org/10.3892/mmr.2015.3192
Pages: 3235-3242
Copyright: © Sun et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

The stem cell populations in cancerous tissues and cell lines vary widely and are often associated with aggressive cases of breast cancer. Despite research on the topic, the mechanism underlying the regulation of the breast cancer stem cell (BCSC) population within tumors remains to be fully elucidated. To investigate the function of special AT‑rich sequence‑binding protein‑1 (SATB1) in the maintenance of the BCSC population, SATB1 was overexpressed with lentivirus in MCF‑7 cells or knocked down with shRNA‑lentivirus in BT‑549 cells. The effects of SATB1 overexpression or knockdown on mammosphere formation, the size of the of BCSC population, cell invasion and tumorigenesis were investigated. Activation of the Notch signaling pathway and expression of Snail1 and Twist1 were also examined in the cells. Overexpression of SATB1 in MCF‑7 cells was observed to increase mammosphere formation, the size of the BCSC population, cell invasion and tumorigenesis, accompanied by an increase in the activation of Notch signaling and expression levels of Snail1 and Twist1. Conversely, knockdown of SATB1 in BT‑549 cells produced the opposite effects. The results indicated that expression of SATB1 may increase the size of the BCSC population via the activation of the Notch signaling pathway and by increasing expression levels of Snail1 and Twist1.

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