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Role of DiGeorge syndrome critical region gene 9, a long noncoding RNA, in gastric cancer

INTRODUCTION: Long non-coding RNAs (lncRNAs) regulate and influence cancer cell development and tumor formation. However, the role for lncRNAs in gastric cancer has not been fully established. In this study, DGCR9, a lncRNA, was significantly upregulated in gastric cancer cell lines. METHODS: The ex...

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Detalles Bibliográficos
Autores principales: Ni, Chao, Yang, Ping, Guo, Junming, Ye, Meng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5914736/
https://www.ncbi.nlm.nih.gov/pubmed/29719408
http://dx.doi.org/10.2147/OTT.S162253
Descripción
Sumario:INTRODUCTION: Long non-coding RNAs (lncRNAs) regulate and influence cancer cell development and tumor formation. However, the role for lncRNAs in gastric cancer has not been fully established. In this study, DGCR9, a lncRNA, was significantly upregulated in gastric cancer cell lines. METHODS: The expression levels of DGCR9 in each patient between formalin-fixed, paraffin-embedded (FFPE) gastric cancer tissues and adjacent noncancer tissues (NAT) (n=102) were measured by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The effect of DGCR9 on cellular proliferation, migration, and glucose uptake was investigated in vitro, respectively. RESULTS: DGCR9 was shown to have increased expression in gastric cancer tissues and in gastric cancer cell lines. Further, DGCR9 was found to be associated with clinicopathological characteristics of patients with gastric cancer. In particular, DGCR9 was positively associated with lymph node invasion and tumor-node-metastasis (TNM) stage in gastric cancer patients. By in vitro functional analysis, knockdown of DGCR9 in gastric cancer cells suppressed cellular proliferation, migration, and glucose uptake. In contrast, overexpression of DGCR9 increased each of these cancer cell characteristics. CONCLUSIONS: DGCR9 was upregulated in gastric cancer tissues and was shown to accelerate cellular proliferation, migration, and glucose metabolism, all of which would promote the formation and development of gastric cancer.