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ChIPseq analysis of changes in binding of TFCP2L1 antibody in B16F0 cells in response to SX-682 treatment.

ABSTRACT: ChIPseq analysis of changes in binding of TFCP2L1 antibody in B16F0 cells in response to SX-682 treatment.

PROVIDER: PRJNA925529 | ENA |

REPOSITORIES: ENA

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ChIPseq analysis of changes in binding of TFCP2L1 antibody in B16F0 cells in response to SX-682 treatment.

Project description:To define the activity of TFCP2L1 following CXCR2 perturbation, we performed chromatin immunoprecipitation and sequencing analysis (CHIPseq) on B16F0 tumorigenic melanoma cells following treatment with vehicle or SX-682.

2023-06-07 | GSE223289 | GEO

Effect of SX-682 treatment on gene expressions of three murine cell lines.

Project description:To identify tumor-specific transcriptional changes following SX-682 treatment, we performed RNA sequencing on each of the MelanA, B16F0, and B16F10 cell lines.

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Effect of SX-682 on gene expression for BrafV600E/PTEN-/- mice.

Project description:To evaluate the effect of the dual CXCR1/CXCR2 inhibitor SX-682 on tumor growth, BrafV600E/PTEN-/- mice were fed with either SX-682 chow (0.756 g/kg of SX-682, Syntrix Pharmaceuticals, Inc) or control chow for RNA-seq analysis.

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Effect of CXCL1 and CXCL1 with SX-682 on gene expression for human epidermal melanocytes (NHEM) cells.

Project description:To gain insight into how CXCL1 activation of CXCR2 regulates the expression of stemness and differentiation markers, RNAseq analysis was performed on normal human epidermal melanocyte (NHEM) cultures treated with CXCL1 or with CXCL1 and SX-682.

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SX-682 and Nivolumab for the Treatment of RAS-Mutated, MSS Unresectable or Metastatic Colorectal Cancer, the STOPTRAFFIC-1 Trial

Project description:This phase Ib/II trial studies the side effects and best dose of SX-682 that can be given alone and in combination with nivolumab in treating patients with RAS-Mutated, microsatellite stable (MSS) colorectal cancer that has spread to other places in the body (metastatic) or cannot be removed by surgery (unresectable). SX-682 may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Immunotherapy with monoclonal antibodies, such as nivolumab, may help the body’s immune system attack the cancer, and may interfere with the ability of tumor cells to grow and spread. Giving SX-682 alone and together with nivolumab may kill more tumor cells.

| 2355422 | ecrin-mdr-crc

Effect of SX-682 on gene expression for BrafV600E/PTEN-/- mice.

Project description:Effect of SX-682 on gene expression for BrafV600E/PTEN-/- mice.

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Effect of SX-682 treatment on gene expressions of three murine cell lines.

Project description:Effect of SX-682 treatment on gene expressions of three murine cell lines.

| PRJNA925528 | ENA

Effect of CXCL1 and CXCL1 with SX-682 on gene expression for human epidermal melanocytes (NHEM) cells.

Project description:Effect of CXCL1 and CXCL1 with SX-682 on gene expression for human epidermal melanocytes (NHEM) cells.

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Identification of CDK1 phosphorylation of TFCP2L1 from murine embryonic stem cells and bladder cancer cells

Project description:Molecular programs involved in embryogenesis are frequently upregulated in oncogenic dedifferentiation and metastasis. However, their precise roles and regulatory mechanisms remain elusive. Here, we showed that CDK1 phosphorylation of TFCP2L1, a pluripotency-associated transcription factor, orchestrated pluripotency and cell-cycling in embryonic stem cells (ESCs) and was aberrantly activated in aggressive bladder cancers (BCs). In murine ESCs, the protein interactome and transcription targets of Tfcp2l1 indicated its involvement in cell-cycle regulation. Tfcp2l1 was phosphorylated at Thr177 by Cdk1, which affected ESC cell-cycle progression, pluripotency, and differentiation. LC-MS was used to characterize thr177 phosphorylation in TFCP2L1 protein obtained by IP experiment and kinase assay. The CDK1-TFCP2L1 pathway was activated in human BC cells, stimulating their proliferation, self-renewal, and invasion. Lack of TFCP2L1 phosphorylation impaired the tumorigenic potency of BC cells in a xenograft model. In patients with BC, high co-expression of TFCP2L1 and CDK1 was associated with unfavorable clinical characteristics including tumor grade, lymphovascular and muscularis propria invasion, and distant metastasis and was an independent prognostic factor for cancer specific survival. These findings demonstrate the molecular and clinical significance of CDK1-mediated TFCP2L1 phosphorylation in stem-cell pluripotency and in the tumorigenic stemness features associated with BC progression.

2019-11-08 | PXD015635 | Pride

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