LncRNA SNHG5 suppresses cell migration and invasion of human lung adenocarcinoma via regulation of epithelial-mesenchymal transition
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ABSTRACT:
PROVIDER: PRJNA601639 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10902576_1.fastq.gz | Fastqsanger.gz | |||
| SRR10902576_2.fastq.gz | Fastqsanger.gz | |||
| SRR10902577_1.fastq.gz | Fastqsanger.gz | |||
| SRR10902577_2.fastq.gz | Fastqsanger.gz | |||
| SRR10902578_1.fastq.gz | Fastqsanger.gz |
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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
Project description:Long noncoding RNAs (lncRNAs) are gradually being annotated as important regulators of multiple cellular processes. The goal of our study was to investigate the effects of the lncRNA small nucleolar RNA host gene 5 (SNHG5) in lung adenocarcinoma (LAD) and its underlying mechanisms. The findings revealed a substantial drop in SNHG5 expression in LAD tissues, which correlated with clinical-pathological parameters. Transcriptome sequencing analysis demonstrated that the inhibitory effect of SNHG5 was associated with cell adhesion molecules. Moreover, the expression of SNHG5 was shown to be correlated with epithelial-mesenchymal transition (EMT) markers in western blots and immunofluorescence. SNHG5 also had significant effects of antimigration and anti-invasion on LAD cells in vitro. Furthermore, the migration and invasion of A549 cells were suppressed by overexpressed SNHG5 in the EMT progress induced by transforming growth factor β1 (TGF-β1), and this might be due to the inhibition of the expression of EMT-associated transcription factors involving Snail, SLUG, and ZEB1. In LAD tissues, the expression of SNHG5 exhibited a positive association with E-cadherin protein expression but a negative correlation with N-cadherin and vimentin, according to the results of quantitative real-time PCR (qRT-PCR). In summary, the current work demonstrated that the lncRNA SNHG5 might limit cell migration and invasion of LAD cancer via decreasing the EMT process, indicating that SNHG5 might be used as a target for LAD therapeutic methods.
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Project description:Glioblastoma cells are characterized by a highly invasive behavior whose mechanisms are not yet understood. Using the wound healing and Boyden chamber assays we compared in the present study the migration and invasion abilities of 5 glioblastoma cell lines (DK-MG, GaMG, U87-MG, U373-MG, SNB19) differing in p53 and PTEN status. We also analyzed by Western blotting the expression of PTEN, p53, mTOR and several other marker proteins involved in cell adhesion, migration and invasion. Among 5 cell lines, GaMG cells exhibited the fastest rate of wound closure, whereas U87-MG cells showed the most rapid chemotactic migration in the Boyden chamber assay. In DK-MG and GaMG cells, F-actin mainly occurred in the numerous stress fibers spanning the cytoplasm, whereas U87-MG, U373-MG and SNB19 cells preferentially expressed F-actin in filopodia and lamellipodia. Moreover, the two glioblastoma lines mutated in both p53 and PTEN genes (U373-MG and SNB19) were found to exhibit the fastest invasion rates through the Matrigel matrix.
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