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Gene expression signatures in GIST-T1 cells transfected with a miR-335 mimic molecule

ABSTRACT: To clarify the effect of miRNAs, we carried out a gene expression microarray analysis using GIST-T1 cells transfected with a miR-335 mimic or a negative control. We found that 1,095 probe sets (853 unique genes) were downregulated (>1.5-fold) by ectopic miR-335 expression. GIST-T1 cells were transfected with a mirVana miR-335 mimic (Ambion) or a mirVana miRNA mimic Negative Control #1 (Ambion). Forty-eight hours after transfection, total RNA extraction was carried out, and gene expression signatures were analyzed.

ORGANISM(S): Homo sapiens

SUBMITTER: Hiromu Suzuki

PROVIDER: E-GEOD-68742 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression signatures in GIST-T1 cells transfected with a miR-34a mimic molecule

Project description:To clarify the effect of miRNAs, we carried out a gene expression microarray analysis using GIST-T1 cells transfected with a miR-34a mimic or a negative control. We found that 2,621 probe sets (1,933 unique genes) were downregulated (>1.5-fold) by ectopic miR-34a expression, including PDGFRA gene which was previously reported as a miR-34a target gene. GIST-T1 cells were transfected with a mirVana miR-34a mimic (Ambion) or mirVana miRNA mimic Negative Control #1 (Ambion). Forty-eight hours after transfection, total RNA extraction was carried out, and gene expression signatures were analyzed.

2015-05-25 | E-GEOD-68740 | biostudies-arrayexpress

Gene expression signatures in GIST-T1 cells transfected with a miR-335 mimic molecule

Project description:To clarify the effect of miRNAs, we carried out a gene expression microarray analysis using GIST-T1 cells transfected with a miR-335 mimic or a negative control. We found that 1,095 probe sets (853 unique genes) were downregulated (>1.5-fold) by ectopic miR-335 expression.

2015-05-25 | GSE68742 | GEO

Gene expression signatures in GIST-T1 cells transfected with siRNA targeting HOTAIR

Project description:To analyze the effect of HOTAIR depletion in a gastrointestinal stromal tumor (GIST) cells, RNAi-mediated knockdown of HOTAIR was carried out using GIST-T1 cells. Gene expression microarray analysis revealed that a number of reported HOTAIR target genes were upregulated by knockdown of HOTAIR. Moreover, we found that 1424 genes were upregulated by siHOT (>2-fold), and Gene Ontology analysis revealed enrichment of genes related to “nucleus”, “chromosome” and “membrane-bounded organelle.” For RNAi-mediated knockdown of HOTAIR, three different Stealth siRNAs against HOTAIR were generated by Invitrogen, after which a mixture of the three was used for transfection. GIST-T1 cells in 6-well plates were transfected with 100 pmol of Stealth siRNA (Invitrogen) or a Stealth RNAi Negative Control Medium GC (Invitrogen) using Lipofectamine2000 (Invitrogen). Total RNA was extracted 48 h after transfection.

2011-12-01 | E-GEOD-32064 | biostudies-arrayexpress

Homo sapiens

Project description:Gene expression signatures in GIST-T1 cells transfected with a miR-335 mimic molecule

| PRJNA283818 | ENA

Project description:Gene expression signatures in GIST-T1 cells transfected with miR-34a and miR-335 mimic molecules

| PRJNA283539 | ENA

Gene expression signatures in GIST-T1 cells transfected with miR-34a and miR-335 mimic molecules

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-05-25 | E-GEOD-68743 | biostudies-arrayexpress

Kinome Profiling of Gastrointestinal Stromal Tumors Using Multiplexed Inhibitor Beads and Mass Spectrometry Identifies Wee1 as a Candidate Therapeutic Target

Project description:Purpose: Management of gastrointestinal stromal tumor (GIST) has been revolutionized by the identification of activating mutations in KIT and PDGFRA and the clinical application of receptor tyrosine kinase (RTK) inhibitors in the advanced disease setting. Stratification of GIST into molecularly defined subsets provides insight into clinical behavior and response to approved targeted therapies. Although these RTK inhibitors are effective in the majority of GIST, resistance to these agents remains a significant clinical obstacle. Development of effective treatment strategies for refractory GIST requires identification of novel targets to provide additional therapeutic options. Global kinome profiling has the potential to identify critical signaling networks and reveal protein kinases that are essential in GIST. Experimental Design: Using Multiplexed Inhibitor Beads and Mass Spectrometry paired with a super-SILAC kinome standard, we explored the majority of the kinome in GIST specimens from three GIST subtypes (KIT-mutant, PDGFRA-mutant and succinate dehydrogenase-deficient GIST) to identify novel kinase targets. In vitro and in vivo studies were performed to evaluate the utility of targeting the identified kinases in GIST. Results: Kinome profiling revealed distinct signatures in three GIST subtypes. PDGFRA-mutant GIST had elevated tumor associated macrophage (TAM) kinases and immunohistochemical analysis confirmed increased TAMs present in these tumors. Kinome profiling with loss-of-function assays revealed a significant role for G2-M tyrosine kinase, Wee1, in GIST survival. In vitro and in vivo studies revealed significant efficacy of MK-1775 (Wee1 inhibitor) in combination with avapritinib in both KIT and PDGFRA-mutant GIST cell lines, as well as notable efficacy of MK-1775 as a single agent in the PDGFRA-mutant line. Conclusions: These studies provide strong preclinical justification for the use of MK-1775 in GIST.

2021-09-09 | PXD020720 | Pride

Gene expression signatures in GIST-T1 cells transfected with a miR-34a mimic molecule

2015-05-25 | GSE68740 | GEO

Gene expression signatures in GIST-T1 cells transfected with a miR-186 inhibitor molecule

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2017-01-01 | GSE85613 | GEO

Restoring miR-150-5p to a triple negative breast cancer cell line [BT-549]

Project description:The objective of these experiments is to identify novel direct and indirect targets of miR-150-5p in breast cancer cell lines. The goal is that these will give direction as to what targets or pathways may be contributing to the reduced growth observed in these cell lines upon restoration of miR-150-5p. A therapy directed towards one or more critical subtype-specific targets could be developed as a therapeutic for breast cancer patients. Using has-miR-150-5p mirVana miRNA mimic (Ambion, 4464066), miR-150-5p was restored to a triple negative breast cancer cell line, BT-549.

2017-01-01 | GSE87589 | GEO

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