当前位置： SCI文献检索 > BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS期刊下所有文献 > Knockdown of long non-coding RNA TUG1 suppresses nasopharyngeal carcinoma progression by inhibiting epithelial-mesenchymal transition (EMT) via the promotion of miR-384.

Knockdown of long non-coding RNA TUG1 suppresses nasopharyngeal carcinoma progression by inhibiting epithelial-mesenchymal transition (EMT) via the promotion of miR-384.

Abstract：

:Nasopharyngeal carcinoma (NPC) is a cancer arising from the nasopharynx epithelium. Long non-coding RNAs (lnc RNA) play a critical role in various biological processes such as cell growth, embryonic development, and tumorigenesis. In the study, for the first time, we discovered that lnc RNA taurine upregulated gene 1 (TUG1) exhibited higher expression levels in NPC tissues and NPC cell lines than in normal nasopharyngeal epithelial tissues and normal nasopharyngeal cell line. In addition, patients with NPCs showing higher levels of TUG1 had worse overall survivals. Further, suppressing TUG1 expression markedly reduced the cell proliferation, migration and invasion; however, TUG1 over-expression significantly enhanced the proliferation, migration and invasion in NPC cells. TUG1 knockdown-inhibited epithelial-mesenchymal transition (EMT) was evidenced by the reduced expression of Vimentin, N-cadherin and transforming growth factor (TGF)-β1, while the enhanced level of E-cadherin. The results of luciferase reporter analysis verified that miR-384 was a direct target of TUG1 in NPC, and was down-regulated in NPC tissues, exhibiting suppressive role in cell proliferation, migration and invasion. In vivo, TUG1 knockdown reduced tumor growth via the regulation of miR-384 by restraining EMT development. In conclusion, our findings suggested that there was a negative correlation between TUG1 and miR-384 in NPC patients. TUG1 might be an effective candidate for use in NPC diagnosis, prognosis and treatment.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Qian W,Ren Z,Lu X

doi

10.1016/j.bbrc.2018.12.011

subject

Has Abstract

pub_date

2019-01-29 00:00:00

pages

56-63

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(18)32654-8

journal_volume

509

pub_type

杂志文章

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