Papillary thyroid cancer cell lines treated with Y15
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Biao Liu
PROVIDER: E-GEOD-55603 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:3 papillary thyroid cancer cell lines were compared, treated with Y15 to untreated.
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Project description:Chromosome 1 open reading frame 106 (C1orf106) has been shown to be elevated in lung adenocarcinoma. However, its expression and function in papillary thyroid cancer (PTC) are totally unknown. To explore the role of C1orf106 in PTC, we analyzed the gene expression in TPC1 cells with or without C1orf106 overexpression.
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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:Purpose: Focal adhesion kinase (FAK), hyaluronan (HA), and hyaluronan synthase-3 (HAS3) have been implicated in cancer growth and progression. FAK inhibition with the small molecule inhibitor Y15 decreases colon cancer cell growth in vitro and in vivo. HAS3 inhibition in colon cancer cells decreases FAK expression and activation, and exogenous HA increases FAK activation. We sought to determine the genes affected by HAS and FAK inhibition and hypothesized that dual inhibition would synergistically inhibit viability. Methods: We treated SW620 colon cancer cells with Y15 to inhibit FAK. We used two strategies to inhibit HAS: (1) cells were transfected with siRNA (HAS3 inhibited); a scrambled sequence was used as a control (HAS3 scrambled), and (2) cells were treated with the HAS inhibitor 4-methylumbelliferone (4-MU). To determine the effect on viability, MTT assays were performed on transfected cells treated with Y15, and wild type cells treated with Y15 alone, 4-MU alone or Y15+4-MU. Treated and untreated cells were submitted to the gene microarray facility for expression profiling. RT-PCR was done to confirm the results. Results: HAS and FAK inhibition affected cell viability. Y15 and 4-MU decreased viability in a dose-dependent manner; viability was further inhibited by treatment with Y15+4-MU in combination (p<0.05). HAS-inhibited cells treated with as little as 2 M of Y15 showed significantly decreased viability compared to HAS scrambled cells treated with the same dose (p<0.05), suggesting synergistic inhibition of viability with dual FAK/HAS inhibition. Microarray analysis showed more than 2-fold up- or down-regulation of 121 genes by HAS inhibition, and 696 genes by FAK inhibition (p<0.05). Of 29 genes that were common to both groups, 9 were down-regulated (CBS, DHRS3, EEPD1, ESPN, FAM46C, GRTP1, IL20RA, INHBE, SCNN1A) and 4 were up-regulated (ANXA1, MALL, RGS2, SNAI2). RT-PCR confirmed these findings. Among the genes affected by FAK or HAS3 inhibition were FOX genes (apoptosis, cell cycle regulation), ANXA1 (apoptosis, proliferation), IL8 (cell cycle regulation, adhesion, proliferation), RGS2 (cell cycle regulation), CEACAM6 (adhesion), SNAI2 (transcription regulation), and SFRP5 (apoptosis). Several genes were specific to either FAK or HAS3 inhibition and several were common to both. Gene expression profiles of samples isolated from human colorectal cancer cells (SW620). A comparison of gene expression between untreated cells and cells treated with 4mcM of Y15. A second comparison between cells transfected with siRNA to HAS3 (HAS3-silenced) and cells transfected with a scrambled control sequence (sc). Two replicates each.
2013-06-01 | E-GEOD-39168 | biostudies-arrayexpress
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2007-07-11 | E-GEOD-3950 | biostudies-arrayexpress
Project description:Global gene expression in TT cells treated with FAK inhibitors TT cells were untreated and treated with Y15 small molecule FAK inhibitor at 10 microM or another FAK inhibitor PF04554878 at 10microM, total RNA was isolated and gene expression was analyzed using Illumina chips
2015-07-03 | E-GEOD-55619 | biostudies-arrayexpress
Project description:We compared the expression profiles of papillary thyroid tumors from the Chernobyl Tissues Bank (CTB) with tumors from French patients with no history of exposure to radiations. Keywords: papillary thyroid cancer vs. patient-matched healthy adjacent thyroid
2007-07-12 | GSE3950 | GEO
Project description:Label-free proteomics profiling of 37 paired tumor-normal tissues of papillary thyroid cancer
2024-02-08 | PXD044900 | Pride