Long noncoding RNA LINC00511 promotes cell growth and invasion in triple-negative breast cancer by interacting with Snail
Authors Liu R, Wang L, Gan T, Pan T, Huang J, Bai M
Received 30 January 2019
Accepted for publication 30 April 2019
Published 24 June 2019 Volume 2019:11 Pages 5691—5699
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Colin Mak
Peer reviewer comments 2
Editor who approved publication: Dr Antonella D'Anneo
This paper has been retracted
Ruilei Liu,1,* Liang Wang,2,* Tianyu Gan,1 Tao Pan,3 Jianglong Huang,4 Mingjun Bai3
1Department of Thyroid and Breast Surgery, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, People’s Republic of China; 2Department of Gastrointestinal Surgery, The First Afﬁliated Hospital, Sun Yat-sen University, Guangzhou, People’s Republic of China; 3Department of Vascular Interventional Radiology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, People’s Republic of China; 4Department of Gastrointestinal Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, People’s Republic of China
*These authors contributed equally to this work
Purpose: Aberrant long noncoding RNA expression has been frequently reported in cancer research, including in triple-negative breast cancer (TNBC). The aim of the present study was to investigate the involvement of LINC00511 in the progression and prognosis of TNBC.
Materials and methods: The expression level of LINC00511 was examined by RT-PCR in TNBC tissues and in cell lines. MTT and colony formation assays were used to examine the cell growth ability. A Boyden assay was used to examine the cell invasion ability. RNA pull-down and RNA immunoprecipitation (RIP) assays were used to examine the proteins that interacted with LINC00511.
Results: We demonstrated that the LINC00511 expression level was elevated in TNBC tissues when compared with that in normal breast tissues. The downregulation of LINC00511 decreased TNBC cell growth and invasion compared to those of the controls. To explore the molecular mechanisms underlying the biological activity of LINC00511, we identified proteins that bound to LINC00511 with RNA pull-down experiments. We showed that LINC00511 binds to the β-transducin repeat containing (BTRC) E3 ubiquitin protein. Mechanistically, LINC00511 maintained the stability of Snail by impeding its ubiquitination and degradation by the BTRC E3 ubiquitin protein.
Conclusion: Our data suggested that LINC00511 might serve as a novel molecular target for the treatment of TNBC.
Keywords: triple-negative breast cancer, LINC00511, Snail
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