MiRNA-101 inhibits breast cancer growth and metastasis by targeting CX chemokine receptor 7

Abstract

// Jun-Tang Li 1, 2, 3, * , Lin-Tao Jia 3, * , Ning-Ning Liu 1, * , Xiao-Shan Zhu 1 , Qin-Qin Liu 1 , Xiu-Li Wang 1 , Feng Yu 1 , Yan-Li Liu 1 , An-Gang Yang 2 , Chun-Fang Gao 1 1 Centre of Inflammation and Cancer Research, 150th Central Hospital of PLA, Luoyang, Henan 471031, China 2 State Key Laboratory of Cancer Biology, Department of Immunology, Fourth Military Medical University, Xi’an, Shaanxi 710032, China 3 State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi’an, Shaanxi 710032, China * These authors have contributed equally to this work Correspondence to: Chun-Fang Gao, e-mail: gaocfsoul@163.com An-Gang Yang, e-mail: agyang@fmmu.edu.cn Keywords: breast cancer, MiR-101, CXCR7, proliferation, metastasis Received: May 13, 2015      Accepted: August 21, 2015      Published: September 01, 2015 ABSTRACT Whereas miR-101 is involved in the development and progression of breast cancer, the underlying molecular mechanisms remain to be elucidated. Here, we report that miR-101 expression is inversely correlated with the clinical stage, lymph node metastasis and prognosis in breast cancers. Introduction of miR-101 inhibited breast cancer cell proliferation and invasion in vitro and suppressed tumor growth and lung metastasis of in vivo . CX chemokine receptor 7 (CXCR7) is a direct target of miR-101, positively correlating with the histological grade and the incidence of lymph node metastasis in breast cancer patients. The effects of miR-101 were mimicked and counteracted by CXCR7 depletion and overexpression, respectively. STAT3 signaling downstream of CXCR7 is involved in miR-101 regulation of breast cancer cell behaviors. These findings have implications for the potential application of miR-101 in breast cancer treatment.