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Gene expression analysis following 24h siRNA-mediated knockdown of transforming growth factor β receptor III (TGFBR3) in human pulmonary arterial endothelial cells (hPAEC).

ABSTRACT: We explored the impact of transforming growth factor β receptor III (TGFBR3) knockdown on the gene expression in the human pulmonary arterial endothelial cells (hPASMC).

ORGANISM(S): Homo sapiens

PROVIDER: GSE92553 | GEO | 2017/12/16

SECONDARY ACCESSION(S): PRJNA358033

REPOSITORIES: GEO

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microRNA expression analysis following 24h siRNA knockdown of transforming growth factor β receptor III (TGFBR3) in human pulmonary arterial smooth muscle cells.

Project description:We explored the impact of transforming growth factor β receptor III (TGFBR3) knockdown on the microRNA expression in the human pulmonary arterial smooth muscle cells (hPASMC), at 24h timepoint.

2017-12-16 | GSE92554 | GEO

Gene expression analysis following 24h- and 48h-siRNA knockdown of transforming growth factor β receptor III (TGFBR3) in human pulmonary arterial smooth muscle cells (hPASMC).

Project description:We explored the impact of siRNA-mediated knockdown of the transforming growth factor β receptor III (TGFBR3) on the gene expression in the human pulmonary arterial smooth muscle cells (hPASMC), at 24h and 48h.

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Gene expression analysis following 6h-, 12h-, 18h- and 24h-siRNA knockdown of transforming growth factor β receptor III (TGFBR3) in human pulmonary arterial smooth muscle cells (hPASMC).

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Expression data from TGFBR3 controls and TGFBR3 knockdown of SUM159 3D cultures

Project description:The objective of this experiment was to determine global gene expression change in triple negative cell line upon knockdown of TGFBR3. Genotype specific differences in expression profiles have been evaluated using human HuGene1.0-ST affymetrix array. RNA was extracted from SUM159 controls and SUM159 TGFBR3KD cells cultured in 3-dimensional in vitro system. Control (N=3) and TGFBR3KD (N=3) samples were hybridized to the Human gene 1.0 ST array, scanned with Affymetrix using AGCC v. 3.2.4 and then analyzed in R 3.0.1 using the oligo package.

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Decreased TGFBR3/Betaglycan expression enhances the metastatic abilities of renal cell carcinoma cells through TGF-b-dependent and independent mechanisms

Project description:It is unclear how the loss of TGF-b signaling components affects metastatic abilities in clear cell renal cell carcinoma (ccRCC). In this study, we identified that low TGFBR3 expression in ccRCC cells enhanced primary tumor formation and lung metastasis. In the presence of TGFBR3, TGF-b2 decreased the aldehyde dehydrogenase (ALDH)-positive ccRCC cell population, in which renal cancer-initiating cells are enriched. Loss of TGFBR3 also enhanced cell migration in cell culture and induced expression of several mesenchymal markers in a TGF-b-independent manner. Increased lamellipodium formation by FAK-PI3K signaling was observed with TGFBR3 downregulation, and this contributed to TGF-b-independent cell migration in ccRCC cells. Taken together, our findings reveal that loss of TGFBR3 endows ccRCC cells with multiple metastatic abilities through TGF-b-dependent and independent pathways.

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Homo sapiens

Project description:Gene expression analysis following 24h- and 48h-siRNA knockdown of transforming growth factor β receptor III (TGFBR3) in human pulmonary arterial smooth muscle cells (hPASMC).

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Project description:Gene expression analysis following 6h-, 12h-, 18h- and 24h-siRNA knockdown of transforming growth factor β receptor III (TGFBR3) in human pulmonary arterial smooth muscle cells (hPASMC).

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Transcriptome data of miR-483 overexpression in human pulmonary arterial endothelial cells

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