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NOTCH1 is a poor prognostic factor for breast cancer and is associated with breast cancer stem cells

Authors Zhong Y, Shen S, Zhou Y, Mao F, Lin Y, Guan J, Xu Y, Zhang S, Liu X, Sun Q

Received 31 March 2016

Accepted for publication 26 July 2016

Published 7 November 2016 Volume 2016:9 Pages 6865—6871


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Cho

Ying Zhong,1 Songjie Shen,1 Yidong Zhou,1 Feng Mao,1 Yan Lin,1 Jinghong Guan,1 Yali Xu,1 Shu Zhang,2 Xu Liu,3 Qiang Sun1

1Department of Breast Disease, 2Department of Dermatology, Peking Union Medical College Hospital, 3Centralab Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, People’s Republic of China

Abstract: Recently, the human gene NOTCH1 has been found to be implicated in cancer cell metastasis and the maintenance of cancer stem cells. However, for breast cancer in particular, an association between NOTCH1 levels and metastasis has not been determined. In this study, we investigated the expression status and correlation of NOTCH1 with clinically important factors related to metastasis and the cancer stem cell marker ALDH1. NOTCH1 and ALDH1 levels in 115 tumor tissues from primary lesions were determined by immunohistochemical staining. Most tissues were stained positive for both NOTCH1 and ALDH1, and NOTCH1 positivity was significantly associated with ALDH1 levels. NOTCH1 levels were significantly associated with TNM stage, metastasis, and triple-negative breast cancer. Moreover, both univariate and multivariate regression analyses revealed that basal-like features and NOTCH1 positivity were associated with disease-free survival as independent predictors. These analyses indicated that breast cancer patients testing positive for NOTCH1 had shorter disease-free survival. Our findings suggest that NOTCH1 may be involved in metastasis and is closely correlated with breast cancer stem cells.

Keywords: breast cancer, NOTCH1, metastasis, ALDH1, cancer stem cell

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