MicroRNA-210 interacts with FBXO31 to regulate cancer proliferation cell cycle and migration in human breast cancer
Dayue Liu,1,* Haoming Xia,1,* Fang Wang,2 Cui Chen,2 Jianting Long2 1Department of Surgery, Breast Disease Center, 2Department of Medicinal Oncology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, People’s Republic of China *These authors contributed equally to&nbs...
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doaj-371c691e2e294a16ad0ecae3dfdc1ef82020-11-24T22:20:26ZengDove Medical PressOncoTargets and Therapy1178-69302016-08-01Volume 95245525528536MicroRNA-210 interacts with FBXO31 to regulate cancer proliferation cell cycle and migration in human breast cancerLiu DXia HWang FChen CLong JDayue Liu,1,* Haoming Xia,1,* Fang Wang,2 Cui Chen,2 Jianting Long2 1Department of Surgery, Breast Disease Center, 2Department of Medicinal Oncology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, People’s Republic of China *These authors contributed equally to this work Background: In this study, we investigated the functional correlation between microRNA-210 (miR-210) and gene of F-box protein 31 (FBXO31) in regulating breast cancer.Methods: Dual-luciferase assay and quantitative real-time polymerase chain reaction were used to investigate the binding of miR-210 with FBXO31 and their expression patterns in breast cancer. miR-210 was inhibited in breast cancer T47D and MCF-7 cells to assess its effect on cancer proliferation, cell cycle progression, and migration. FBXO31 was also downregulated in breast cancer cells to examine its effect on miR-210-mediated breast cancer regulation. The interaction between miR-210 and FBXO31 was further investigated by examining the effect of overexpressing miR-210 on FBXO31-induced suppression of breast cancer proliferation.Results: FBXO31 was the downstream target gene of miR-210 in breast cancer. miR-210 and FBXO31 are inversely expressed in breast cancer cell lines. miR-210 downregulation reduced cancer progression, induced cell cycle arrest, and inhibited cancer migration in T47D and MCF-7 cells. Tumor suppression by miR-210 downregulation was reversed by downregulating FBXO31. In FBXO31-overexpressed breast cancer cells, upregulating miR-210 also reversed the tumor-suppressive effect of FBXO31 on breast cancer proliferation.Conclusion: Our work demonstrated that the expression pattern and tumor regulatory functions of miR-210 and FBXO31 are inversely correlated in breast cancer. Keywords: breast cancer, miR-210, FBXO31, cancer proliferation, cancer migrationhttps://www.dovepress.com/microrna-210-interacts-with-fbxo31-to-regulate-cancer-proliferation-ce-peer-reviewed-article-OTTBreast cancermiR-210FBXO31cancer proliferationcancer migration |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Liu D Xia H Wang F Chen C Long J |
spellingShingle |
Liu D Xia H Wang F Chen C Long J MicroRNA-210 interacts with FBXO31 to regulate cancer proliferation cell cycle and migration in human breast cancer OncoTargets and Therapy Breast cancer miR-210 FBXO31 cancer proliferation cancer migration |
author_facet |
Liu D Xia H Wang F Chen C Long J |
author_sort |
Liu D |
title |
MicroRNA-210 interacts with FBXO31 to regulate cancer proliferation cell cycle and migration in human breast cancer |
title_short |
MicroRNA-210 interacts with FBXO31 to regulate cancer proliferation cell cycle and migration in human breast cancer |
title_full |
MicroRNA-210 interacts with FBXO31 to regulate cancer proliferation cell cycle and migration in human breast cancer |
title_fullStr |
MicroRNA-210 interacts with FBXO31 to regulate cancer proliferation cell cycle and migration in human breast cancer |
title_full_unstemmed |
MicroRNA-210 interacts with FBXO31 to regulate cancer proliferation cell cycle and migration in human breast cancer |
title_sort |
microrna-210 interacts with fbxo31 to regulate cancer proliferation cell cycle and migration in human breast cancer |
publisher |
Dove Medical Press |
series |
OncoTargets and Therapy |
issn |
1178-6930 |
publishDate |
2016-08-01 |
description |
Dayue Liu,1,* Haoming Xia,1,* Fang Wang,2 Cui Chen,2 Jianting Long2 1Department of Surgery, Breast Disease Center, 2Department of Medicinal Oncology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, People’s Republic of China *These authors contributed equally to this work Background: In this study, we investigated the functional correlation between microRNA-210 (miR-210) and gene of F-box protein 31 (FBXO31) in regulating breast cancer.Methods: Dual-luciferase assay and quantitative real-time polymerase chain reaction were used to investigate the binding of miR-210 with FBXO31 and their expression patterns in breast cancer. miR-210 was inhibited in breast cancer T47D and MCF-7 cells to assess its effect on cancer proliferation, cell cycle progression, and migration. FBXO31 was also downregulated in breast cancer cells to examine its effect on miR-210-mediated breast cancer regulation. The interaction between miR-210 and FBXO31 was further investigated by examining the effect of overexpressing miR-210 on FBXO31-induced suppression of breast cancer proliferation.Results: FBXO31 was the downstream target gene of miR-210 in breast cancer. miR-210 and FBXO31 are inversely expressed in breast cancer cell lines. miR-210 downregulation reduced cancer progression, induced cell cycle arrest, and inhibited cancer migration in T47D and MCF-7 cells. Tumor suppression by miR-210 downregulation was reversed by downregulating FBXO31. In FBXO31-overexpressed breast cancer cells, upregulating miR-210 also reversed the tumor-suppressive effect of FBXO31 on breast cancer proliferation.Conclusion: Our work demonstrated that the expression pattern and tumor regulatory functions of miR-210 and FBXO31 are inversely correlated in breast cancer. Keywords: breast cancer, miR-210, FBXO31, cancer proliferation, cancer migration |
topic |
Breast cancer miR-210 FBXO31 cancer proliferation cancer migration |
url |
https://www.dovepress.com/microrna-210-interacts-with-fbxo31-to-regulate-cancer-proliferation-ce-peer-reviewed-article-OTT |
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