Gene and microRNA expression changes induced by overexpression of SphK1 in papillary thyroid cancer cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE87312 | GEO | 2016/09/24
SECONDARY ACCESSION(S): PRJNA344302
REPOSITORIES: GEO
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Project description:The oncogenic roles of Sphingosine kinase 1 (SphK1) in various cancers, including thyroid cancer, have been well demonstrated. However, miRNAs associated with the oncogenic roles of SphK1 remains largely unknown. The goal of this study is to detect the global gene and microRNA (miRNA) expression in response to Sphk1 over-expression and identify potential therapeutic targets. To achieve this, SphK1 was stably overexpressed in papillary thyroid cancer cell line TPC1. Then the mRNA and miRNA expression were quantified using digital gene expression (DGE) analysis and small RNA-seq in TPC1-Vector and TPC1-SphK1 cells, respectively. miRNA-mRNA interactions were explored by microT-CDS and the predicted networks were visualized using CytoScape. In this study, we found that over-expression of SphK1 differentially regulates 46 miRNA and 506 mRNAs expression in TPC1 cells. Combining bioinformatics prediction of mRNA targets and DGE data on mRNA expressions allowed to identify mRNA targets of deregulated miRNAs. The direct interaction between miR-144-3p and FN1 mRNA, which mediates the pro-invasive role of SphK1 in thyroid cancer cells, was experimentally validated. In general, our results provided a miRNA-mRNA regulatory network in response to SphK1 overexpression in thyroid cancer cells. We also demonstrated a role of miR-144-3p and FN1 in mediating oncogenic function of SphK1, which enhance the understanding of etiology of thyroid cancer.
2016-09-24 | GSE87310 | GEO
Project description:The oncogenic roles of Sphingosine kinase 1 (SphK1) in various cancers, including thyroid cancer, have been well demonstrated. However, miRNAs associated with the oncogenic roles of SphK1 remains largely unknown. The goal of this study is to detect the global gene and microRNA (miRNA) expression in response to Sphk1 over-expression and identify potential therapeutic targets. To achieve this, SphK1 was stably overexpressed in papillary thyroid cancer cell line TPC1. Then the mRNA and miRNA expression were quantified using digital gene expression (DGE) analysis and small RNA-seq in TPC1-Vector and TPC1-SphK1 cells, respectively. miRNA-mRNA interactions were explored by microT-CDS and the predicted networks were visualized using CytoScape. In this study, we found that over-expression of SphK1 differentially regulates 46 miRNAs and 506 mRNAs expression in TPC1 cells. Combining bioinformatics prediction of mRNA targets and DGE data on mRNA expressions allowed to identify mRNA targets of deregulated miRNAs. The direct interaction between miR-144-3p and FN1 mRNA, which mediates the pro-invasive role of SphK1 in thyroid cancer cells, was experimentally validated. In general, our results provided a miRNA-mRNA regulatory network in response to SphK1 overexpression in thyroid cancer cells. We also demonstrated a role of miR-144-3p and FN1 in mediating oncogenic function of SphK1, which enhance the understanding of etiology of thyroid cancer.
2016-09-24 | GSE87307 | GEO
Project description:Gene and microRNA expression changes induced by overexpression of SphK1 in papillary thyroid cancer cells
| PRJNA344302 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2014-06-30 | E-GEOD-49415 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2014-06-30 | GSE49415 | GEO
Project description:OBJECTIVES:Papillary thyroid cancer (PTC) is the most common subtype of thyroid cancer, which accounts for 80-90% of all thyroid cancer cases. Though the pathological mechanism hasn't been fully understood, it is reported that both environmental and genetic factor may contribute to the PTC susceptibility. MicroRNAs (miRNAs) are small non-coding RNA molecules which function as the suppressors to participate in a variety of biological processes. Accumulating evidence suggests that polymorphisms of miRNAs were associated with the tumorigenesis of various cancers, including PTC. In this article, we focus on the association between four common microRNA polymorphisms (miR-146a, miR-608, miR-933, and miR-149) and PTC risk in a Han Chinese population. METHODS:In this case-control study, we recruited 1,398 participants in total, including 369 PTC patients, 278 patients with thyroid benign nodules (BN) and 751 normal controls. The miRNAs polymorphisms were genotyped and analyzed by using MALDI-TOF mass spectrometry. The odd ratios and their 95% confidence interval (95% CI) were calculated to evaluate the association between miRNAs polymorphisms and PTC risk. Furthermore, a meta-analysis based on previous studies was conducted to comprehensively assess the diagnostic performance of miR-146a in the PTC diagnosis. RESULTS:The miR-146a polymorphisms were shown to be significantly correlated with elevated risk of PTC under the heterozygous, homozygous, dominant and allelic models by comparing the genotype distribution between PTC cases and healthy controls, as well as between PTC cases and BN cases. However, the result of meta-analysis showed no significant association between miR-146a polymorphisms and PTC risk. CONCLUSIONS:Our study indicated that the miR-146a polymorphism was significantly associated with PTC risk. In contrast, meta-analysis revealed no evidence of association between miR-146a variants and PTC risk. Further studies are required to elucidate the role of miR-146a in the etiology of PTC.
| S-EPMC4680501 | biostudies-literature
Project description:ObjectivesPapillary thyroid cancer (PTC) is increasing in incidence. Fine needle aspiration is the gold standard for diagnosis, but results can be indeterminate. Identifying tissue and serum biomarkers, like microRNA, is therefore desirable. We sought to identify miRNA that is differentially expressed in the serum of patients with PTC.MethodsSerum miRNA was quantified in 31 female thyroidectomy patients: 13 with benign disease and 18 with PTC. qPCR results were compared for significant fold-changes in 175 miRNAs, against a pooled control.Results128 miRNA qualified for analysis. There were identifiable fold-changes in miRNA levels between benign and control, and between PTC and control. There were statistically significant fold changes in the level of four miRNAs between benign and PTC: hsa-miR-146a-5p and hsa-miR-199b-3p were down-regulated, while hsa-let7b-5p and hsa-miR-10a-5p were up-regulated.ConclusionsMicroRNA is differentially expressed in the serum of patients with PTC. Serum miRNA has the potential to aid in thyroid cancer diagnosis.
| S-EPMC4560924 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2014-01-07 | E-GEOD-42395 | biostudies-arrayexpress
Project description:Label-free proteomics profiling of 37 paired tumor-normal tissues of papillary thyroid cancer
2024-02-08 | PXD044900 | Pride
Project description:Kruppel-like factor 4 (KLF4) has been implicated in a number of different types of cancer; however, the role of KLF4 in papillary thyroid cancer remains elusive. The present study aimed to investigate the role of KLF4 in papillary thyroid cancer and its potential underlying molecular mechanisms. The expression of KLF4 in thyroid tumor tissue and adjacent non-cancerous tissues were detected via immunohistochemistry and western blotting. The papillary thyroid cancer cell line, KTC1, was transfected with viruses carrying KLF4 overexpression vectors. The relative expression of KLF4, E-cadherin, N-cadherin, Vimentin, matrix metalloproteinase (MMP)2, MMP9 and collagen was detected via quantitative-PCR. The viability of KTC1 cells was detected using a cell counting kit-8 assay at 24, 48 and 72 h. Cell invasion was examined via a transwell invasion assay. Cell migration was examined via a scratch migration assay at 0 and 24 h. Compared with adjacent non-cancerous tissues, the expression of KLF4 was significantly lower in thyroid tumor tissues. The expression of KLF4 in KTC1 cells were significantly increased compared with the blank or negative control groups. The expression of N-cadherin, MMP2, MMP9 and collagen was significantly decreased in the KLF4 overexpression group. The viability of KTC1 cells was markedly decreased in KLF4 overexpression group at 24, 48 and 72 h when compared with the blank or negative control groups. The invasion of KTC1 cells in the KLF4 overexpression group was markedly decreased. Compared with the negative control group, the KTC1 cell migration in the KLF4 overexpression group was markedly decreased at 24 h. The expression of KLF4 was also significantly lower in thyroid tumor tissues. The cell viability, tumor invasion and migration ability and expression levels of N-cadherin, MMP2, MMP9 and collagen in papillary thyroid cancer cells were markedly decreased with KLF4 overexpression.
| S-EPMC6777314 | biostudies-literature