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SNHG5 promotes colorectal cancer cell survival by counteracting STAU1-mediated mRNA destabilization

ABSTRACT: We functionally characterize SNHG5 as an important lncRNA, which could constitute a new therapeutic target in colorectal cancer, and provide a novel mechanism of action for a cytoplasmic lncRNA

ORGANISM(S): Homo sapiens

PROVIDER: GSE76792 | GEO | 2017/01/01

SECONDARY ACCESSION(S): PRJNA308594

REPOSITORIES: GEO

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SNHG5 promotes colorectal cancer cell survival by counteracting STAU1-mediated mRNA destabilization.

Project description:We currently have limited knowledge of the involvement of long non-coding RNAs (lncRNAs) in normal cellular processes and pathologies. Here, we identify and characterize SNHG5 as a stable cytoplasmic lncRNA with up-regulated expression in colorectal cancer. Depletion of SNHG5 induces cell cycle arrest and apoptosis in vitro and limits tumour outgrowth in vivo, whereas SNHG5 overexpression counteracts oxaliplatin-induced apoptosis. Using an unbiased approach, we identify 121 transcript sites interacting with SNHG5 in the cytoplasm. Importantly, knockdown of key SNHG5 target transcripts, including SPATS2, induces apoptosis and thus mimics the effect seen following SNHG5 depletion. Mechanistically, we suggest that SNHG5 stabilizes the target transcripts by blocking their degradation by STAU1. Accordingly, depletion of STAU1 rescues the apoptosis induced after SNHG5 knockdown. Hence, we characterize SNHG5 as a lncRNA promoting tumour cell survival in colorectal cancer and delineate a novel mechanism in which a cytoplasmic lncRNA functions through blocking the action of STAU1.

| S-EPMC5192221 | biostudies-literature

LncRNA SNHG5 suppresses cell migration and invasion of human lung adenocarcinoma via regulation of epithelial-mesenchymal transition

Project description:Long noncoding RNAs (lncRNAs) are emerging as important regulators in cellular processes. In the present study, the effects of the long non-coding RNA, SNHG5 was investigated in lung adenocarcinoma (LAD) and we also revealed the underlying mechanisms of it. Overexpressed SNHG5 suppressed migration and invasion of LAD cell line A549 in vitro. Transcriptome sequencing analysis supported the inhibitory effects of SNHG5 were associated with cell adhesion molecules. In addition, western blot and immunofluorescence showed that the expression of SNHG5 was associated with epithelial-mesenchymal transition (EMT) markers. Furthermore, we determined the effects of SNHG5 in EMT procession of A549 induced by TGF-β1. Consistent with previous results, overexpression of SNHG5 suppressed the migration and invasion, and also the expression of EMT-related transcription factors including Snail, SLUG and ZEB1 in EMT of A549 reduced by TGF-β1. Moreover, qRT-PCR demonstrated expression of SNHG5 was positively correlated with E-cadherin protein expression, but negatively correlated with N-cadherin and Vimentin in LAD tissues. In summary, our study demonstrated that lncRNA SNHG5 could suppress cell migration and invasion of LAD cancer by inhibiting EMT procession, highlighting the potential of SNHG5 as a therapy strategy for lung adenocarcinoma.

2020-01-17 | GSE143766 | GEO

Loss of Snhg5 disrupts cell-cycle regulation without altering cystogenesis in a mouse model of polycystic kidney disease.

Project description:Long non-coding RNAs (lncRNAs) regulate diverse cellular pathways and are increasingly linked to human disease. Snhg5 is frequently described as a pathogenic lncRNA in many human diseases, including cancer. Our previous studies revealed that Snhg5 is one of the most upregulated lncRNAs in multiple mouse models of polycystic kidney disease (PKD). Yet its role in renal biology and in autosomal dominant PKD (ADPKD) is not known. To elucidate the role of Snhg5, we generated a global Snhg5-null mouse. Homozygous animals were viable and displayed normal kidney morphology and function. RNA-sequencing of Snhg5-null kidneys and renal epithelial cells revealed common alterations in gene expression linked to cell cycle progression and DNA replication. At the molecular level, Snhg5-null cells showed an increased mitotic fraction, coinciding with depletion of ARPC5—a core ARP2/3 subunit— suggesting that reduced ARPC5 may contribute to this phenotype. To determine whether Snhg5 upregulation is pathogenic in mouse PKD, we crossed Snhg5-null mice with a collecting duct-specific Pkd1-mutant mouse model. Loss of Snhg5 did not attenuate cyst formation; if anything, disease severity was mildly but not significantly exacerbated. These findings indicate that Snhg5 modulates mitotic control and is dispensable for kidney development and cystogenesis in collecting duct-derived cysts.

2025-06-30 | GSE300255 | GEO

SNHG5 siRNA knock down in HCT116 cells

Project description:SnoRNA host gene 5 was knocked down with two different siRNAs and profiled for gene expression. three replicates of two different siRNAs against SNHG5 and a control siRNA

2016-04-01 | E-GEOD-76801 | biostudies-arrayexpress

LncRNA SNHG5 adversely governs follicular growth in PCOS via miR-92a-3p/CDKN1C axis

Project description:Small nucleolar RNA host genes (SNHGs) have been implicated in various biological processes, yet their involvement in polycystic ovary syndrome (PCOS) remains elusive. Specifically, SNHG5, a long non-coding RNA implicated in several human cancers, shows elevated expression in granulosa cells (GCs) of PCOS women and induces PCOS-like features when overexpressed in mice. In vitro, SNHG5 inhibits GC proliferation and induces apoptosis and cell cycle arrest at G0/G1 phase, with RNA-seq indicating its impact on DNA replication and repair pathways. Mechanistically, SNHG5 acts as a competing endogenous RNA by binding to miR-92a-3p, leading to increased expression of target gene CDKN1C, which further suppresses GC proliferation and promotes apoptosis. These findings elucidate the crucial role of SNHG5 in the pathogenesis of PCOS and suggest a potential therapeutic target for this condition. Additional investigations such as large-scale clinical studies and functional assays are warranted to validate and expand upon these findings.

2023-11-05 | GSE246995 | GEO

Expression analysis of gene expression changes in Homo sapiens SGC-7901 cells after knock down of MTA2 or overexpression of SNHG5

2015-09-09 | GSE65915 | GEO

Expression analysis of gene expression changes in Homo sapiens SGC-7901 cells after knock down of MTA2 or overexpression of SNHG5

Project description:Expression analysis of gene expression changes in Homo sapiens SGC-7901 cells after knock down of MTA2 (Metastasis-associated protein) or overexpression SNHG5 (snoRNA host gene 5) Investigation of whole genome gene expression level changes in a Homo sapiens gastric carcinoma cells SGC-7901 after knock down MTA2 expression and upregulation of SNHG5 A four chip study using total RNA extracted from SGC-7901 cells transfected with siRNA negative control and SGC-7901 cells knock down of MTA2 with siRNA. Each chip measures the expression level of 45033 genes collected from the authoritative data source including NCBI

2015-09-09 | E-GEOD-65915 | biostudies-arrayexpress

LncRNA SNHG5 adversely governs follicular growth in PCOS via miR-92a-3p/CDKN1C axis

Project description:LncRNA SNHG5 adversely governs follicular growth in PCOS via miR-92a-3p/CDKN1C axis

| PRJNA1035508 | ENA

LncRNA SNHG5 suppresses cell migration and invasion of human lung adenocarcinoma via regulation of epithelial-mesenchymal transition

Project description:LncRNA SNHG5 suppresses cell migration and invasion of human lung adenocarcinoma via regulation of epithelial-mesenchymal transition

| PRJNA601639 | ENA

LncRNA LIMp27 regulates the DNA damage response through p27 in p53-defective cancer cells

Project description:P53 inactivation occurs in about 50% of human cancers, where p53-driven p21 activity is devoid and p27 becomes essential for the establishment of the G1/S checkpoint upon DNA damage. Here, we show that the E2F1-responsive lncRNA LIMp27 selectively represses p27 expression and contributes to proliferation, tumorigenicity, and treatment resistance in p53-defective colon adenocarcinoma (COAD) cells. LIMp27 competes with p27 mRNA for binding to cytoplasmically localized hnRNA0, which otherwise stabilizes p27 mRNA leading to cell cycle arrest at the G0/G1 phase. In response to DNA damage, LIMp27 is upregulated in both wild-type and p53-mutant COAD cells, whereas cytoplasmic hnRNPA0 is only increased in p53-mutant COAD cells due to translocation from the nucleus. Moreover, high LIMp27 expression is associated with poor survival of p53-mutant but not wild-type p53 COAD patients. These results uncover a lncRNA mechanism that promotes p53-defective cancer pathogenesis and suggest that LIMp27 may constitute a target for the treatment of such cancers.

| MSV000090292 | MassIVE

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