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The Long Noncoding RNA SNHG1 Regulates Both the Local and Distal Genes in Cancer

ABSTRACT: Many long noncoding transcripts are involved in cancer progression. Here, we utilized high-throughput microarray to compare the transcriptome alterations between the SNHG1 knockdown or control in HCT116 cell lines. Two independent siRNAs were designed against the SNHG1 cDNA sequence. Thus, we identified 302 genes which were expressionally changed. Moreover, Gene Ontology and pathway enrichment analysis revealed that several gene signature were significantly enriched, such as MAPK signaling pathway, growth factor activity and transcriptional corepresssor activity. Further, GSEA analysis suggested NF-kB signaling pathway, PI3K/Akt pathway were markedly associated with SNHG1-reuglated genes. The present study indicated that SNGH1 regulated both the local and distal genes in cancer progression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE69843 | GEO | 2015/10/01

SECONDARY ACCESSION(S): PRJNA286906

REPOSITORIES: GEO

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Project description:Neuroblastoma (NB) is an embryonal tumor with various clinical presentations and behaviors. Several genomic alterations has been well-studied in NB, among which genomic amplification of MYCN oncogene, is a strong prognostic biomarker with worsens outcome. Long noncoding RNAs (lncRNAs), constitute major proportion of the cellular transcripts with no coding capacity. One of their function is to guide transcription factors to the target genes and facilitate gene expression. However, relative contribution of lncRNA and MYCN to the advanced NB has remained unclear. Herein, by applying a network-based integrative analysis on MYCN amplified and MYCN nonamplified lncRNA expression profile from both RNA-seq and microarray platform, we identified lncRNA, SNHG1 to be differentially expressed and strongly correlated with MYCN in MYCN-amplified NB. The expression of SNHG1 was validated by RT-qPCR in NB cell lines. Survival analysis revealed that higher expression of SNHG1 significantly associates with poor patient survival. Moreover, knockdown of MYCN in MYCN-amplified NB cell lines inhibited SNHG1 expression. Furthermore, to unravel the role of SNHG1 in NB, we extracted SNHG1-interacting proteins by RNA-protein pull down assay coupled with doi:10.6342/NTU201701980 ! ! VI liquid chromatography-tandem mass spectrometry (LC-MS/MS). We identified 27 SNHG1-interacting proteins in common from three NB cell lines. However, only three SNHG1-interacting proteins, MATR3, YBX1 and HHRNPL have binding site detected by DeepBind motif analysis. Western blot confirms interaction of MATR3 with SNHG1. Additionally, we further validated the direct interaction between MATR3 and SNHG1 by RNA-immunoprecipation (IP). MATR3 is known to be involved in RNA transport and stabilization. Therefore, we proposed that MATR3 after interacting with SNHG1 might help in SNHG1 transcription and stabilization. In conclusion, our study unveils that SNHG1 could be a prognostic marker for high-risk NB and possibly stabilized by MATR3. Our results might provide future directions for the development of therapeutic strategies against high-risk NB.

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The Long Noncoding RNA SNHG1 Regulates Both the Local and Distal Genes in Cancer

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