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Expression data from C42B prostate cancer cell line treated with enzalutamide and/or sphingosine kinase inhibitor PF-543 or ABC294640

ABSTRACT: Expression data from C42B prostate cancer cell line treated with enzalutamide and/or sphingosine kinase inhibitor PF-543 or ABC294640

PROVIDER: PRJNA727461 | ENA |

REPOSITORIES: ENA

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Expression data from C42B prostate cancer cell line treated with enzalutamide and/or sphingosine kinase inhibitor PF-543 or ABC294640

Project description:Epidemiological and molecular evidence indicate that sphingolipids may play a role in the resistance of prostate cancer to androgen receptor signalling inhibitors such as enzalutamide, through the metabolism of ceramide into sphingosine-1-phosphate (S1P) which activates specific G-protein coupled receptors present on cancer cells and immune cells. Sphingosine kinase inhibitors which prevent the production of S1P have anti-cancer effects in vitro and in animal models. Our work showed that SPHK inhibitors can enhance the efficacy of enzalutamide in prostate cancer cell lines. We used microarrays to investigate the transcriptomic changes from the combination of enzalutamide with the SPHK1 inhibitor PF543, or SPHK2 inhibitor ABC294640, in C42B, one of the prostate cancer cell line.

2021-10-14 | GSE173886 | GEO

Crystal Structure of Sphingosine Kinase 1 with PF-543.

Project description: Not available

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Impact of Sphingosine Kinase-1 knock out in neonatal mice lungs

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2016-10-30 | GSE87350 | GEO

Verification of the Necessity of the Tolyl Group of PF-543 for Sphingosine Kinase 1 Inhibitory Activity.

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Sphingosine kinase 1 regulates the pulmonary vascular immune response

Project description:Sphingosine kinase 1 regulates the pulmonary vascular immune response

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Sphingosine kinase 1 regulates the pulmonary vascular immune response

Project description:Aberrant proliferation of pulmonary arterial smooth muscle (PASMCs) cells are a defining characteristic of pulmonary arterial hypertension (PAH) and leads to increased vascular resistance, elevated pulmonary pressure, and right heart failure. The Sphingosine kinase 1 (SPHK1)/Sphingosine-1 phosphate/ Sphingosine-1 phosphate receptor 2 pathway promotes vascular remodeling and induces PAH. The aim of this study was to identify genes and cellular processes that are modulated by over-expression of SPHK1 in human PASMCs (hPASMCs). RNA was purified and submitted for RNA sequencing to identify differentially expressed genes. Using a corrected p-value threshold of <0.05, there were 294 genes significantly up-regulated while 179 were significantly down-regulated. Predicted effects of these differentially expressed genes was evaluated using the freeware tool Enrichr to assess general gene set over-representation (enrichment) and Ingenuity Pathway Analysis (IPA™) for upstream regulator predictions. We found a strong change in genes that regulated the cellular immune response. IL6, STAT1, and PARP9, were elevated in response to SPHK1 over-expression in hPASMCs. The gene set enrichment mapped to a few immune modulatory signaling networks, including IFNG. Furthermore, STAT1 protein was elevated in primary hPASMCs isolated from PAH patients. In conclusion, these data suggest a role of Sphk1 regulates pulmonary vascular immune response in PAH.

2021-06-22 | GSE174304 | GEO

NOTCH signaling is activated in and contributes to resistance in enzalutamide-resistant prostate cancer cells

Project description:Prostate cancer is the second leading cause of cancer death among men in the United States. The Androgen receptor (AR) antagonist Enzalutamide is a FDA approved therapy for treatment of late stage prostate cancer patients and is currently under clinical study for early stage prostate cancer treatment. After a short positive response period, patients will develop drug resistance. In this study we used RNA-sequencing and bioinformatics analysis to identify Notch signaling pathway as a deregulated pathway in Enzalutamide-resistant cells. NOTCH2 and c-MYC positively correlated with AR expression in patients' samples mimicking cells with Enzalutamide-resistance. In Enzalutamide-resistant cells, MR49F and C4-2R, we found that cleaved-NOTCH1, HES1 and c-MYC protein expression are significantly elevated indicating an activated NOTCH1 pathway in those cells. In addition, ADAM10 and ADAM17 had a higher expression in Enzalutamide-resistant cells, suggesting a role for S2 cleavage in the increased cleaved NOTCH1 expression. Furthermore, treatment of Enzalutamide-resistant cells with PF-03084014 in combination with Enzalutamide increased cell death, decreased colony formation ability and re-sensitized Enzalutamide-resistant cells to Enzalutamide. Knockdown of NOTCH1 in C4-2R increases Enzalutamide sensitivity by decreasing cell proliferation and increasing cell death. In a 22RV1 xenograft model, PF-03084014 and Enzalutamide induced a decrease in tumor growth through a reduced cell proliferation and increased apoptosis. These results indicate that Notch1 signaling can contribute to Enzalutamide-resistance in Prostate cancer and inhibition of this pathway can re-sensitize resistant cells to Enzalutamide.

2019-04-01 | GSE123379 | GEO

Proteomics of murine melanoma tumor cells upon sphingosine kinase-1 inhibition

Project description:In order to assess the impact of sphingosine kinase-1 (SK1) expression on melanoma growth, stable SK1 knockdown cells were generated by shRNA, using Yumm 1.7 cells derived from spontaneous murine melanoma driven by Braf activation as well as Pten and Cdkn2a inactivation. Two cell lines silenced for SK1 (shSK1(1) and shSK1(2)) were obtained.

2019-12-17 | PXD016535 | Pride

Expression data from prostate cancer cell lines C4-2B (enzalutamide sensitive) and C4-2B-MDVR (enzalutamide resistant) cells

Project description:Prostate cancer C4-2B cells were cultured in enzalutamide in a dose-escalation manner. After sixty passages cells were resistant to enzalutamide, with a specific sets of genes been deregulated. We performed global gene expression analysis by cDNA microarrays to identify genes responsible for enzalutamide resistance in C4-2B-MDVR cells. Enzalutamide resistant C4-2B-MDVR cells were selected from C4-2B cells during long time enzalutamide treatment. Genes responsible for enzalutamide resistance were identified using C4-2B vs. C4-2B-MDVR RNA extraction and hybridization on Affymetrix microarrays.

2015-04-09 | E-GEOD-64143 | biostudies-arrayexpress

Sphingosine kinase 2 in stromal fibroblasts creates a hospitable tumor microenvironment in breast cancer

Project description:Reciprocal interactions between breast cancer cells and the tumor microenvironment are important for cancer progression and metastasis. We report here that the deletion or inhibition of sphingosine kinase 2 (SphK2), which produces sphingosine-1-phosphate (S1P), markedly suppresses syngeneic breast tumor growth and lung metastasis in mice by creating a hostile microenvironment for tumor growth and invasion. SphK2 deficiency decreased S1P and concomitantly increased ceramides, including C16-ceramide, in stromal fibroblasts. Ceramide accumulation suppressed activation of cancer-associated fibroblasts (CAFs) by upregulating stromal p53, which restrained production of tumor-promoting factors to reprogram the tumor microenvironment and restrict breast cancer establishment. Ablation of p53 in SphK2-deficient fibroblasts reversed these effects, enabled CAF activation and promoted tumor growth and invasion. These data uncovered a novel role of SphK2 in regulating non-cell autonomous functions of p53 in stromal fibroblasts and their transition to tumor-promoting CAFs, paving the way for the development of a strategy to target the tumor microenvironment and enhance therapeutic efficacy.

2020-01-01 | GSE136655 | GEO

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