Abstract
BackgroundRecent evidence indicates that long noncoding RNAs (lncRNAs) play pivotal roles in the regulation of cellular processes and are found to be dysregulated in a variety of cancers. LINC00261 is an lncRNA that is aberrantly expressed in gastric cancer (GC). The clinical role of LINC00261 in GC and molecular mechanisms remains to be found.MethodsReal-time polymerase chain reaction (PCR) was used to examine LINC00261 expression in GC cell lines/tissues compared with normal epithelial cells/adjacent non-tumorous tissues. Gain and loss of function approaches were used to investigate the biological role of LINC00261 in GC cells. The effects of LINC00261 on cell viability were evaluated by MTT and colony formation assays. Wound healing assay, cell migration and invasion assays, and nude mice were used to examine the effects of LINC00261 on tumor cell metastasis in vitro and in vivo. Protein levels of LINC00261 targets were determined by western blot and immunohistochemistry.ResultsLINC00261 was downregulated in GC cell lines and cancerous tissues, as compared with normal gastric epithelial cells and adjacent noncancerous tissue samples. Low LINC00261 expression was correlated with deeper tumor invasion (P < 0.001), higher tumor stage (P = 0.013), and lymphatic metastasis (P = 0.006). Univariate and multivariate analyses indicated that low LINC00261 expression predicted poor prognosis. Ectopic expression of LINC00261 impaired cell migration and invasion, leading to the inhibition of metastasis in vitro and in vivo. Knockdown of LINC00261 expression promoted cell migration and invasion in vitro. Overexpression of LINC00261 was found to play a key role in epithelial–mesenchymal transition (EMT) through the regulation of E-cadherin, N-cadherin, and Vimentin expression.ConclusionsLow expression of the lncRNA LINC00261 occurs in GC and is associated with poor prognosis. LINC00261 suppresses GC metastasis by regulating EMT. Thus, LINC00261 plays an important role in the progression and metastasis of GC.Electronic supplementary materialThe online version of this article (doi:10.1186/s13045-016-0288-8) contains supplementary material, which is available to authorized users.
Highlights
Recent evidence indicates that long noncoding RNAs play pivotal roles in the regulation ofR cellular processes and are found to be dysregulated in a variety of cancers
C LINC00261 contributes to invasion and metastasis in I gastric cancer (GC), we investigated potential target proteins involved in ART cell motility and matrix invasion
Our results indicated that LINC00261 mediated inhibi- To gain further insight into the biologic pathways intory effects on GC cell metastasis suppression, possibly volved in GC pathogenesis through LINC00261 pathway, by affecting the epithelial–mesenchymal transition (EMT)
Summary
Recent evidence indicates that long noncoding RNAs (lncRNAs) play pivotal roles in the regulation ofR cellular processes and are found to be dysregulated in a variety of cancers. The clinical stage, based on the TNM classification system, at the time of diagnosis is currently the most important prognostic factor, and the molecular mechanism involved in the progression and metastasis of GC remains unknown [4]. Apart from about 2 % protein-coding genes, more than 90 % of the genome is transcribed as noncoding RNAs (ncRNAs), indicating that ncRNAs could play significant regulatory roles in complex organisms [5, 6]. One subcategory of these transcripts, called long noncoding RNAs (lncRNAs), comprises ncRNAs that are more than 200 nucleotides in length. Accumulating evidence demonstrates that lncRNAs play roles in a variety
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