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Long non-coding RNA NEAT1 regulates E2F3 expression by competitively binding to miR-377 in non-small cell lung cancer.
Zhang, Junsheng; Li, Yongli; Dong, Mei; Wu, Dongyuan.
Afiliação
  • Zhang J; College of Basic Medicine, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
  • Li Y; Department of Pharmacy, The General Hospital of Heilongjiang, Harbin, Heilongjiang 150043, P.R. China.
  • Dong M; Department of Pharmacy, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150040, P.R. China.
  • Wu D; Department of Pharmacy, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150040, P.R. China.
Oncol Lett ; 14(4): 4983-4988, 2017 Oct.
Article em En | MEDLINE | ID: mdl-29085511
ABSTRACT
It has previously been demonstrated that the long non-coding RNA (lncRNA) nuclear enriched abundant transcript (NEAT)-1 is increased in multiple cancers and may be associated with cancer development. However, the function and mechanism of NEAT1 in non-small cell lung cancer (NSCLC) has not yet been fully elucidated. In the present study, the expression of NEAT1 in NSCLC was detected using quantitative polymerase chain reaction and association with survival was estimated. The effect of NEAT1 on proliferation was detected by growth curve and cell cycle analysis. Bioinformatics analysis was used to identify miRNAs that interact with NEAT1. Following this, a series of molecular biological techniques were used to verify the mechanism of NEAT1. The results indicated that NEAT1 was highly expressed in NSCLC, and high NEAT1 expression was associated with a shorter overall survival. NEAT1 promoted NSCLC cell growth and affected the cell cycle process in vitro. Furthermore, NEAT1 was observed to bind hsa-miR-377-3p, functioning as a competing endogenous RNA, which resulted in de-repression of its target gene E2F transcription factor 3 (E2F3). E2F3, as an oncogene, may promote NSCLC progression. These results suggested that NEAT1 may promote the development of NSCLC through the miR-377-3p-E2F3 pathway.
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Texto completo: 1 Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Idioma: En Ano de publicação: 2017 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Idioma: En Ano de publicação: 2017 Tipo de documento: Article