GSE1 negative regulation by miR-489-5p promotes breast cancer cell proliferation and invasion

被引：40

作者：

Chai, Peng ^{[1
]}

Tian, Jingzhong ^{[1
]}

Zhao, Deyin ^{[4
]}

Zhang, Hongyan ^{[1
]}

Cui, Jian ^{[1
]}

Ding, Keshuo ^{[3
]}

Liu, Bin ^{[2
]}

机构：

[1] Peoples Hosp Bozhou, Dept Gen Surg, Bozhou 236800, Peoples R China

[2] Anhui Med Univ, Affiliated Hosp 1, Dept Vasc Surg, Hefei 230022, Peoples R China

[3] Anhui Med Univ, Dept Pathol, Hefei 230022, Peoples R China

[4] Hosp Suzhou, Dept Gen Surg, Suzhou 234000, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2016年 / 471卷 / 01期

关键词：

Breast cancer; GSE1; miRNA; Proliferation; Migration; Invasion; REVEALS; GROWTH;

D O I：

10.1016/j.bbrc.2016.01.168

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Gse1 coiled-coil protein (GSE1), also known as KIAA0182, is a proline rich protein. However, the function of GSE1 is largely unknown. In this study, we reported that GSE1 is overexpression in breast cancer and silencing of GSE1 significantly suppressed breast cancer cells proliferation, migration and invasion. Furthermore, GSE1 was identified as a direct target of miR-489-5p, which is significantly reduced in breast cancer tissues. In addition, forced expression of miR-489-5p suppressed breast cancer cells proliferation, migration and invasion. Moreover, depletion of GSE1 by siRNAs significantly abrogated the enhanced proliferation, migration and invasion of breast cancer cells consequent to miR-489-5p depletion. Taken together, these findings suggest that GSE1 may function as a novel oncogene in breast cancer and it can be regulated by miR-489-5p. (C) 2016 Elsevier Inc. All rights reserved.

引用

页码：123 / 128

页数：6

共 18 条

[1] Predicting effective microRNA target sites in mammalian mRNAs [J].

Agarwal, Vikram ;

Bell, George W. ;

Nam, Jin-Wu ;

Bartel, David P. .

ELIFE, 2015, 4

[2] The molecular pathology of breast cancer progression [J].

Bombonati, Alessandro ;

Sgroi, Dennis C. .

JOURNAL OF PATHOLOGY, 2011, 223 (02) :307-317

[3] The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups [J].

Curtis, Christina ;

Shah, Sohrab P. ;

Chin, Suet-Feung ;

Turashvili, Gulisa ;

Rueda, Oscar M. ;

Dunning, Mark J. ;

Speed, Doug ;

Lynch, Andy G. ;

Samarajiwa, Shamith ;

Yuan, Yinyin ;

Graef, Stefan ;

Ha, Gavin ;

Haffari, Gholamreza ;

Bashashati, Ali ;

Russell, Roslin ;

McKinney, Steven ;

Langerod, Anita ;

Green, Andrew ;

Provenzano, Elena ;

Wishart, Gordon ;

Pinder, Sarah ;

Watson, Peter ;

Markowetz, Florian ;

Murphy, Leigh ;

Ellis, Ian ;

Purushotham, Arnie ;

Borresen-Dale, Anne-Lise ;

Brenton, James D. ;

Tavare, Simon ;

Caldas, Carlos ;

Aparicio, Samuel .

NATURE, 2012, 486 (7403) :346-352

[4]

Dalmay T, 2013, ESSAYS BIOCHEM, V54, P29, DOI [10.1042/bse0540029, 10.1042/BSE0540029]

[5] A candidate X-linked mental retardation gene is a component of a new family of histone deacetylase-containing complexes [J].

Hakimi, MA ;

Dong, Y ;

Lane, WS ;

Speicher, DW ;

Shiekhattar, R .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (09) :7234-7239

[6] MicroRNA gene expression deregulation in human breast cancer [J].

Iorio, MV ;

Ferracin, M ;

Liu, CG ;

Veronese, A ;

Spizzo, R ;

Sabbioni, S ;

Magri, E ;

Pedriali, M ;

Fabbri, M ;

Campiglio, M ;

Ménard, S ;

Palazzo, JP ;

Rosenberg, A ;

Musiani, P ;

Volinia, S ;

Nenci, I ;

Calin, GA ;

Querzoli, P ;

Negrini, M ;

Croce, CM .

CANCER RESEARCH, 2005, 65 (16) :7065-7070

[7] MiR-489 regulates chemoresistance in breast cancer via epithelial mesenchymal transition pathway [J].

Jiang, Li ;

He, Dongxu ;

Yang, Dantong ;

Chen, Zhen ;

Pan, Qiongxi ;

Mao, Aiqin ;

Cai, Yanfei ;

Li, Xiyuan ;

Xing, Hui ;

Shi, Mei ;

Chen, Yun ;

Bruce, Iain C. ;

Wang, Teng ;

Jin, Linfang ;

Qi, Xiaowei ;

Hua, Dong ;

Jin, Jian ;

Ma, Xin .

FEBS LETTERS, 2014, 588 (11) :2009-2015

[8] miR-489 is a tumour-suppressive miRNA target PTPN11 in hypopharyngeal squamous cell carcinoma (HSCC) [J].

Kikkawa, N. ;

Hanazawa, T. ;

Fujimura, L. ;

Nohata, N. ;

Suzuki, H. ;

Chazono, H. ;

Sakurai, D. ;

Horiguchi, S. ;

Okamoto, Y. ;

Seki, N. .

BRITISH JOURNAL OF CANCER, 2010, 103 (06) :877-884

[9] Breast cancer stem cells, EMT and therapeutic targets [J].

Kotiyal, Srishti ;

Bhattacharya, Susinjan .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2014, 453 (01) :112-116

[10] MiR-183/-96/-182 cluster is up-regulated in most breast cancers and increases cell proliferation and migration [J].

Li, Pei ;

Sheng, Cheng ;

Huang, Lingling ;

Zhang, Hui ;

Huang, Lihua ;

Cheng, Zeneng ;

Zhu, Qubo .

BREAST CANCER RESEARCH, 2014, 16 (06)

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