LncRNA SNHG17 contributes to proliferation, migration and poor prognosis of hepatocellular carcinoma
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ABSTRACT:
PROVIDER: PRJNA638818 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11996457_1.fastq.gz | Fastqsanger.gz | |||
| SRR11996457_2.fastq.gz | Fastqsanger.gz | |||
| SRR11996458_1.fastq.gz | Fastqsanger.gz | |||
| SRR11996458_2.fastq.gz | Fastqsanger.gz | |||
| SRR11996459_1.fastq.gz | Fastqsanger.gz |
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Project description:Long noncoding RNAs (lncRNAs) have been substantially reported to have critical roles in regulating tumorigenesis recent years. However, the expression pattern and biological function of SNHG17 in hepatocellular carcinoma (HCC) remain unclearly. Bioinformatics analysis and qRT-PCR were performed to detect the expression pattern of SNHG17 in HCC tissues, adjacent non-tumorous tissues and cell lines. The effect of SNHG17 on proliferation, migration and apoptosis of HCC were investigated by knockdown and overexpressing SNHG17 in HCC cell lines. RNA sequencing was utilized to explore the underlying mechanism. Utilizing publicly available TCGA-LIHC, GSE102079 HCC datasets and qRT-PCR, we found SNHG17 was significantly upregulated in HCC tissues and cell lines and was notably associated with larger tumor size, poorly differentiation, presence of vascular invasion and advanced TNM stage. Furthermore, gain- and loss-of-function studies demonstrated that SNHG17 promoted cell proliferation, migration and inhibited apoptosis of HCC. By employing RNA sequencing, we found knockdown of SNHG17 caused 1037 differentially expressed genes, highly enriched in several pathways, including metabolic, PI3K-Akt, cell adhesion, regulation of cell proliferation and apoptotic pathway, among them 92 were overlapped with SNHG17-related genes in TCGA-LIHC dataset. Furthermore, ERH, TBCA, TDO2 and PDK4 were successfully validated and found significantly dysregulated in HCC tissues. Moreover, HCC patients with higher SNHG17 expression had a relatively poor overall survival and disease-free survival and ERH, PDK4 also played markedly role in prognosis of HCC. Broadly, our findings illustrate that SNHG17 acts as a noncoding oncogene in HCC progression, suggesting its potential value as a novel target for HCC therapy.
2021-09-12 | GSE152256 | GEO
Project description:Long noncoding RNAs (lncRNAs) have been substantially reported to have critical roles in regulating tumorigenesis in recent years. However, the expression pattern and biological function of SNHG17 in hepatocellular carcinoma (HCC) remain unclear. Bioinformatics analysis and qRT-PCR were performed to detect the expression pattern of SNHG17 in HCC tissues, adjacent nontumorous tissues, and cell lines. The effect of SNHG17 on proliferation, migration, and apoptosis of HCC was investigated by knockdown and overexpressing SNHG17 in HCC cell lines. RNA sequencing was utilized to explore the underlying mechanism. Utilizing publicly available TCGA-LIHC, GSE102079 HCC datasets, and qRT-PCR, we found SNHG17 was significantly upregulated in HCC tissues and cell lines and was notably associated with larger tumor size, poorly differentiation, presence of vascular invasion, and advanced TNM stage. Furthermore, gain- and loss-of-function studies demonstrated that SNHG17 promoted cell proliferation and migration and inhibited apoptosis of HCC. By employing RNA sequencing, we found knockdown of SNHG17 caused 1037 differentially expressed genes, highly enriched in several pathways, including metabolic, PI3K-Akt, cell adhesion, regulation of cell proliferation, and apoptotic pathway; among them, 92 were overlapped with SNHG17-related genes in the TCGA-LIHC dataset. Furthermore, ERH, TBCA, TDO2, and PDK4 were successfully validated and found significantly dysregulated in HCC tissues. Moreover, HCC patients with higher SNHG17 expression had a relatively poor overall survival and disease-free survival, and ERH and PDK4 also played a marked role in the prognosis of HCC. Broadly, our findings illustrate that SNHG17 acts as a noncoding oncogene in HCC progression, suggesting its potential value as a novel target for HCC therapy.
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Project description:MicroRNAs are important cellular components and their dysfunctions are associated with various disease.Small-cell lung cancer (SCLC) is an aggressive disease with a poor prognosis, but little is know about the underlying machinery that leads to rapid tumor growth and early metastases.In this study, clinical outcome prediction miRNAs were successfully found through expression profiling of a total of 924 miRNA genes in 42 SCLC cases.
2011-02-22 | GSE27435 | GEO
Project description:MicroRNAs are important cellular components and their dysfunctions are associated with various disease.Small-cell lung cancer (SCLC) is an aggressive disease with a poor prognosis, but little is know about the underlying machinery that leads to rapid tumor growth and early metastases.In this study, clinical outcome prediction miRNAs were successfully found through expression profiling of a total of 924 miRNA genes in 42 SCLC cases. 42 patients with respectable very limited disease (training set) were enrolled. All the patients underwent surgical resection followed by adjuvant chemotherapy according to the standard of care. Total RNA was extracted from formalin-fixed paraffin-embedded （FFPE）specimens, low molecular weight RNA was seperate and labeled , and then hybridized to capitalbio V3 biochip representing about 924 microRNA . three chip were test in each group, and the procedure was repeated twice.
2011-02-22 | E-GEOD-27435 | biostudies-arrayexpress
Project description:Cancer tissue specimens from ARID1Ahigh and good prognosis and ARID1Alow and poor prognosis of patients with advanced gastric cancer were extracted and analyzed.
2018-02-06 | GSE110078 | GEO
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Project description:The prognostic biomarkers and potential therapy targets are urgently needed in hepatocellular carcinoma (HCC). In this article, we report the expression of TUBA1C was significantly increased in HCC on mRNA and protein level, and this finding was further validated in another two independent datasets. Survival analysis was also implemented on these three datasets, and TUBA1C high expression group was detected to have relative shorter survival time. Furthermore, the metastatic ability is increased along with TUBA1C abundance, according to protein abundance evaluation of normal-tumor-portal vein tumor thrombus pairs, and mRNA comparison between metastasis-averse HCC and metastasis-incline HCC. Correlation analysis was implemented and TUBA1C expression was shown to be significantly associated with recurrence, embolus, and AFP level. Proliferation and migration assays following knock down of TUBA1C in two cell lines, HCCLM3 and PLC, revealed that down-regulation of TUBA1C significantly reduces proliferation and migration in HCC cells. in vivo study also showed the similar results. Gene Set Enrichment Analysis (GSEA) comparing the TUBA1C-low and TUBA1C-high group indicates that KEGG pathways including "cell cycle", "DNA replication", and "proteasome" were significantly enriched in TUBA1C-high group. In conclusion, prognostic biomarker and oncogene TUBA1C promotes migration and proliferation of hepatocellular carcinoma cells, probability via cell cycle signaling pathway.
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Project description:MYC regulation of a "poor prognosis" metastatic cancer cell state
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Project description:Background - Hepatocellular carcinomas (HCCs) are heterogeneous tumors with respect to etiology, cell of origin and biology. The course of the disease is unpredictable and is in part dependent on the tumor microenvironment. One of the microenvironmental factors is hypoxia, which is known to promote aggressiveness in other malignant tumors. We hypothesized that certain regions in HCC exist with chronic hypoxia and a characteristic gene expression pattern. Moreover, during the development of HCC there is an important contribution of this chronic hypoxia on prognosis via this gene expression. Until now, most research has been performed in acute hypoxic models (< 24 hours). Methods – Human hepatoblastoma cells HepG2 were cultured in either normoxic (20% O2) or hypoxic (2% O2) conditions for 72 hrs, the time it takes to adapt to chronic hypoxia. After 3 days the cells were harvested and analyzed by microarray technology. The highly significant differentially expressed genes were selected and used to assess the clinical value of our in vitro chronic hypoxia gene signature in four published patient studies. Three of these independent microarray studies on HCC patients were used as training sets to determine a minimal prognostic gene set and one study was used for validation. Gene expression analysis and correlation with clinical outcome was assessed with the bioinfomatic method of Goeman et al (). Results – In the HepG2 cells, 3592 genes were differentially expressed in cells cultured at 2% oxygen for 72 hrs. Out of these, 265 showed a high significant change (2-fold change and p=0.0001). The level of gene expression after 72 hrs was different from the acute hypoxic response (during the first 24 hours) and represented chronicity. Using computational methods we identified 7 out of the 265 highly significant genes that showed correlation with prognosis in all three different training sets and this was independently validated in a 4th dataset. With our approach we could include the largest number of HCC patients in one single study. Conclusion – We identified a 7-gene signature, which is associated with chronic hypoxia and predicts prognosis in patients with HCC. In the future this signature could be used as a diagnostic tool. In addition, chronic hypoxia gene expression information can be used in the search for new therapeutic targets. Two conditions were compared and each sample has a biological replicate. Samples are hybridized in dye-swap, resulting in 4 hybridizations.
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