MiRNA-101 inhibits breast cancer growth and metastasis by targeting CX chemokine receptor 7
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Jun-Tang Li1,2,3,*, Lin-Tao Jia3,*, Ning-Ning Liu1,*, Xiao-Shan Zhu1, Qin-Qin Liu1, Xiu-Li Wang1, Feng Yu1, Yan-Li Liu1, An-Gang Yang2, Chun-Fang Gao1
1Centre of Inflammation and Cancer Research, 150th Central Hospital of PLA, Luoyang, Henan 471031, China
2State Key Laboratory of Cancer Biology, Department of Immunology, Fourth Military Medical University, Xi’an, Shaanxi 710032, China
3State 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
Chun-Fang Gao, e-mail: firstname.lastname@example.org
An-Gang Yang, e-mail: email@example.com
Keywords: breast cancer, MiR-101, CXCR7, proliferation, metastasis
Received: May 13, 2015 Accepted: August 21, 2015 Published: September 01, 2015
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.
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