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Tumor Biology
Published in: Tumor Biology 6/2013

01-12-2013 | Research Article

Effects of ARHI on breast cancer cell biological behavior regulated by microRNA-221

Authors: Ying Li, Mei Liu, Yanjun Zhang, Chun Han, Junhao You, Junlan Yang, Cheng Cao, Shunchang Jiao

Published in: Tumor Biology | Issue 6/2013

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Abstract

The aplysia ras homolog member I (ARHI) is a tumor suppressor gene and is downregulated in various cancers. The downregulation of ARHI was regulated by miR-221 in prostate cancer cell lines. However, it has not been reported whether ARHI is regulated by miR-221 in breast cancer. Here, we reported that the ARHI protein level was downregulated in breast cancer tissues and breast cancer cell lines. The overexpression of ARHI could inhibit cell proliferation and invasion and induce cell apoptosis. To address whether ARHI is regulated by miR-221 in breast cancer cell lines, the results in this study showed that a significant inverse correlation existed between ARHI and miR-221. MiR-221 displayed an upregulation in breast cancer tissues and breast cancer cell lines. The inhibition of miR-221 induced a significant upregulation of ARHI in MCF-7 cells. To prove a direct interaction between miR-221 and ARHI mRNA, ARHI 3′UTR, which includes the potential target site for miR-221, was cloned downstream of the luciferase reporter gene of the pMIR-REPORT vector to generate the pMIR-ARHI-3′UTR vector. The results confirmed a direct interaction of miR-221 with a target site on the 3′UTR of ARHI. In conclusion, ARHI is a tumor suppressor gene that is downregulated in breast cancer. The overexpression of ARHI could inhibit breast cancer cell proliferation and invasion and induce cell apoptosis. This study demonstrated for the first time that the downregulation of ARHI in breast cancer cells could be regulated by miR-221.
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Metadata
Title
Effects of ARHI on breast cancer cell biological behavior regulated by microRNA-221
Authors
Ying Li
Mei Liu
Yanjun Zhang
Chun Han
Junhao You
Junlan Yang
Cheng Cao
Shunchang Jiao
Publication date
01-12-2013
Publisher
Springer Netherlands
Published in
Tumor Biology / Issue 6/2013
Print ISSN: 1010-4283
Electronic ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-013-0933-6

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