Authors

Yuan Li, Research Center for Translational Medicine, Key Laboratory of Arrhythmias of the Ministry of Education, Tongji University School of Medicine, 150 Jimo Road, Shanghai 200120, Chin
Chunli Liang, Research Center for Translational Medicine, Key Laboratory of Arrhythmias of the Ministry of Education, Tongji University School of Medicine, 150 Jimo Road, Shanghai 200120, Chin
Haizhong Ma, Research Center for Translational Medicine, Key Laboratory of Arrhythmias of the Ministry of Education, Tongji University School of Medicine, 150 Jimo Road, Shanghai 200120, China; Lanzhou University School of Pharmacy, First Affiliated Hospital of Lanzhou University, Lanzhou, Gansu 730000, China
Qian Zhao, Research Center for Translational Medicine, Key Laboratory of Arrhythmias of the Ministry of Education, Tongji University School of Medicine, 150 Jimo Road, Shanghai 200120, China
Ying Lu, Research Center for Translational Medicine, Key Laboratory of Arrhythmias of the Ministry of Education, Tongji University School of Medicine, 150 Jimo Road, Shanghai 200120, China
Zhendong Xiang, Research Center for Translational Medicine, Key Laboratory of Arrhythmias of the Ministry of Education, Tongji University School of Medicine, 150 Jimo Road, Shanghai 200120, China
Li Li, Research Center for Translational Medicine, Key Laboratory of Arrhythmias of the Ministry of Education, Tongji University School of Medicine, 150 Jimo Road, Shanghai 200120, China
Jie Qin, Department of Anatomy, Histology and Embryology, Shanghai Medical College, Fudan University, Shanghai 200120, China
Yihan Chen, Research Center for Translational Medicine, Key Laboratory of Arrhythmias of the Ministry of Education, Tongji University School of Medicine, 150 Jimo Road, Shanghai 200120, China
William C Cho, Department of Clinical Oncology, Queen Elizabeth Hospital, Hong Kong, Hong Kong
Richard G Pestell, Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, United StatesFollow
Li Liang, Lanzhou University School of Pharmacy, First Affiliated Hospital of Lanzhou University, Lanzhou, Gansu 730000, China
Zuoren Yu, Research Center for Translational Medicine, Key Laboratory of Arrhythmias of the Ministry of Education, Tongji University School of Medicine, 150 Jimo Road, Shanghai 200120, China

Document Type

Article

Publication Date

6-1-2014

Comments

This article has been peer reviewed. It was published in: Molecules.

Volume 19, Issue 6, June 2014, Pages 7122-7137.

The published version is available at DOI: 10.3390/molecules19067122

Copyright © 2014 by the authors.

Abstract

The miR-221/222 cluster has been demonstrated to function as oncomiR in human cancers. miR-221/222 promotes epithelial-to-mesenchymal transition (EMT) and confers tamoxifen resistance in breast cancer. However, the effects and mechanisms by which miR-221/222 regulates breast cancer aggressiveness remain unclear. Here we detected a much higher expression of miR-221/222 in highly invasive basal-like breast cancer (BLBC) cells than that in non-invasive luminal cells. A microRNA dataset from breast cancer patients indicated an elevated expression of miR-221/222 in BLBC subtype. S-phase entry of the cell cycle was associated with the induction of miR-221/222 expression. miRNA inhibitors specially targeting miR-221 or miR-222 both significantly suppressed cellular migration, invasion and G1/S transition of the cell cycle in BLBC cell types. Proteomic analysis demonstrated the down-regulation of two tumor suppressor genes, suppressor of cytokine signaling 1 (SOCS1) and cyclin-dependent kinase inhibit 1B (CDKN1B), by miR-221/222. This is the first report to reveal miR-221/222 regulation of G1/S transition of the cell cycle. These findings demonstrate that miR-221/222 contribute to the aggressiveness in control of BLBC.

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