RRC ID 56020
著者 Hong Y, He H, Sui W, Zhang J, Zhang S, Yang D.
タイトル Long non-coding RNA H1 promotes cell proliferation and invasion by acting as a ceRNA of miR‑138 and releasing EZH2 in oral squamous cell carcinoma.
ジャーナル Int J Oncol
Abstract Long non-coding RNAs (lncRNAs) have been shown to play pivotal roles in various types of human cancer, including oral squamous cell carcinoma (OSCC). However, the potential mechanisms of action of lncRNAs in OSCC remain to be fully elucidated. The aim of the present study was to further explore the potential mechanisms of action of lncRNAs in OSCC. We first analyzed Gene Expression Omnibus (GEO) datasets to investigate aberrantly expressed lncRNAs which may be involved in the development of OSCC. Reverse transcription‑quantitative PCR (RT‑qPCR) was performed to analyze the expression levels of lncRNA H19. In addition, the correlation between H19 expression and the clinical characteristics and prognosis of patients with OSCC was statistically analyzed. The effects of H19 expression on OSCC cells were examined by using overexpression and RNA interference approaches in vitro and in vivo. To examine the competitive endogenous RNA (ceRNA) mechanisms, bioinformatics analysis and luciferase reporter assay were performed. In addition, the correlation between H19 and microRNA (miR)‑138 was detected. H19 was found to be upregulated in OSCC tissues and its high expression level was associated with the TNM stage and nodal invasion, and also correlated with a shorter overall survival of patients with OSCC. The knockdown of H19 significantly inhibited OSCC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT), and induced apoptosis in vitro; it also suppressed subcutaneous tumor growth in vivo. In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR‑138; the inhibition of miR‑138 attenuated the inhibitory effects of H19 knockdown on OSCC cells. On the whole, our findings suggest that H19 functions as an oncogene by inhibiting miR‑138 and facilitating EZH2 expression in OSCC. Thus, lncRNA H1 may represent a potential therapeutic target for OSCC.
巻・号 52(3)
ページ 901-912
公開日 2018-3-1
DOI 10.3892/ijo.2018.4247
PMID 29344674
MeSH Animals Carcinoma, Squamous Cell / genetics* Carcinoma, Squamous Cell / mortality Carcinoma, Squamous Cell / pathology Cell Line, Tumor Cell Proliferation / genetics Enhancer of Zeste Homolog 2 Protein / genetics* Enhancer of Zeste Homolog 2 Protein / metabolism Female Gene Expression Profiling / methods Gene Knockdown Techniques Humans Male Mice Mice, Inbred BALB C Mice, Nude MicroRNAs / genetics* MicroRNAs / metabolism Middle Aged Mouth Neoplasms / genetics* Mouth Neoplasms / mortality Mouth Neoplasms / pathology Neoplasm Invasiveness / genetics Neoplasm Staging RNA, Long Noncoding / genetics RNA, Long Noncoding / metabolism* RNA, Small Interfering / metabolism Survival Analysis Xenograft Model Antitumor Assays
IF 3.571
引用数 19
リソース情報
ヒト・動物細胞 HSC-3(RCB1975) HSC-2(RCB1945)