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Transcriptomic profiling of SUM-LM1 human breast cancer cells upon treatment with recombinant Activin B or vehicle

ABSTRACT: Transcriptomic profiling of SUM-LM1 human breast cancer cells upon treatment with recombinant Activin B or vehicle

PROVIDER: PRJNA657598 | ENA |

REPOSITORIES: ENA

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Transcriptomic profiling of SUM-LM1 human breast cancer cells upon treatment with recombinant Activin B or vehicle

Project description:In cancer progression to metastasis, disseminated cancer cells frequently lodge near vasculature in secondary organs. However, our understanding of the cellular crosstalk evoked at perivascular sites is still rudimentary. In this study, we identified an inter-cellular machinery governing formation of a pro-metastatic vascular niche during breast cancer colonization in lungs. Transcriptomic analysis of endothelial cells (ECs) isolated from mouse lungs with metastases revealed a marked upregulation of genes linked to proliferation, inflammation and numerous secreted proteins. We showed that four secreted factors, INHBB, SCGB3A1, OPG and LAMA1, induced in ECs form a supportive niche that promotes metastasis in mice, by enhancing stem cell properties and survival ability of cancer cells. Interestingly, the blocking vascular endothelial cell growth factor (VEGF), a major cytokine regulating EC behaviors, dramatically suppressed EC proliferation whereas no impact was observed on the expression of the four vascular niche factors in lung ECs. We found that the formation of a vascular niche is correlated with inflammation, and revealed that metastasis-associated macrophages are essential for production of all of four niche factors in lung ECs. Macrophages are activated via TNC-TLR4 at perivasculature and sequentially stimulate ECs to produce the four niche factors. Thus, our findings provide mechanistic insights into the formation of a perivascular niche and offer the possibility that targeting macrophages may synergize with existing anti-angiogenic drugs to effectively suppress vascular function in metastatic colonization. We used microarrays to analyze the global changes of gene expression in SUM-LM1 human breast cancer cells upon treatment with Activin B

2021-12-31 | GSE156353 | GEO

Transcriptomic profiling of CXCR3+/- SUM-159-LM1 breast cancer cells

Project description:Transcriptomic profiling of CXCR3+/- SUM-159-LM1 breast cancer cells

| PRJNA499116 | ENA

Rhodoligotrophos defluvii strain:lm1

Project description:Rhodoligotrophos- lm1 Assembly

| PRJNA529329 | ENA

Transcription profiling of Lbeta T2 cells treated with either vehicle or activin A for different length of time to characterize the upregulation of gene expression by activin A.

Project description:The primary response of Lbeta T 2cells upon activin treatment at 1hr, 2hr, and 6hr is the significant up-regulation of FSHbeta subunit. Affymetrix genearray missed this important information due to cross-hybridization of its probes with other genes and chromosome segments. Activin modulates a network of genes and signaling pathways to exert a variety of functions. Experiment Overall Design: Subconfluent Lbeta T2 cells were seeded in cell culture flasks for 16 hours in phenol-free, serum-free medium, and then treated with either vehicle or activin A (30ng/ml). At 1hr, 2hr, or 6hr after treatment, total RNA was isolated using RNeasy Mini Kit. Integrity of RNA was evaluated with an Agilent 2100 Bioanalyzer, and purity/concentration was determined using a GeneSpec III before target preparationi and hybridizations.

2007-11-27 | E-GEOD-5232 | biostudies-arrayexpress

Limosilactobacillus mucosae LM1

Project description:Limosilactobacillus mucosae LM1 Genome sequencing

| PRJNA80653 | ENA

Innate triggering and antiviral effector functions of activin A

Project description:Transcriptomic analyses delineated strikingly congruent patterns of gene regulation in hepatocytes stimulated with recombinant activin A and IFNα in vitro. Activin A mRNA, encoded by the INHBA gene, is induced upon activation of RIG-I, MDA5 and TLR7/8 viral nucleic acid sensors in vitro, across multiple cell lines and also in human peripheral blood mononuclear cells

2021-12-08 | GSE190277 | GEO

Marinobacter sp. LM1

Project description:Marinobacter sp. LM1 Genome sequencing and assembly

| PRJNA909479 | ENA

Limosilactobacillus mucosae LM1

Project description:Genome sequencing of Lactobacillus mucosae strain LM1

| PRJNA274438 | ENA

Aquaspirillum sp. LM1

Project description:Aquaspirillum sp. LM1 Genome sequencing and assembly

| PRJNA363092 | ENA

Activin/Nodal signaling in mouse embryonic stem cells

Project description:Members of the transforming growth factor (TGF)-β superfamily play essential roles in the pluripotency, self-renewal, and differentiation of embryonic stem cells. While bone morphogenic proteins maintain pluripotency of undifferentiated mouse ES cells, the role of Activin/Nodal signaling is less clear. To determine the target genes of Activin/Nodal-Smad2 signaling in undifferentiated embryonic stem cells, changes in gene expression were examined following stimulation with recombinant Activin (2 hours) or after inhibition of Activin/Nodal with SB431542 (24 hours) using defined media culture conditions with LIF and 20 ng/mL BMP4. SB431542 is a specific inhibitor of ALK4/5/7 receptors and antagonizes both Activin and Nodal signaling. Via western analysis, Activin stimulation increased pSmad2 in ES cells after 2 hours, and treatment with SB431542 for 24 hours virtually eliminated pSmad2. Total Smad2 expression remained unchanged through these manipulations. RNA from cells treated with Activin or SB431542 was extracted by standard methods with Qiagen RNeasy columns. The RNA was analyzed with the Mouse Genome 430A Array from Affymetrix. Samples were performed in duplicate, and RNA from cells treated with Activin or SB431542 was compared to untreated embryonic stem cells.

2009-08-31 | GSE17879 | GEO

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