WT BMDM M2 vs RON TK- BMDM M2
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ABSTRACT:
PROVIDER: PRJNA701293 | ENA |
REPOSITORIES: ENA
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Project description:Introduction: HGFL-Ron signaling is augmented in human breast cancer and is associated with poor overall prognosis. Here, we investigate the role of HGFL-Ron signaling in RON-modulated murine macrophages through RNA-sequencing of bone marrow-derived macrophages from FVB WT or FVB RON tyrosine kinase -/- mice. BMDM of each genotype M2-polarized via 72 hour treatment with IL-4 were submitted for transcriptomic characterization on the Illumina HiSeq 2500. High quality reads were aligned to the mm10 genome and quantified to generate RPKM
2021-08-10 | GSE166575 | GEO
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Project description:Pancreatic cancer-derived cells NP-18 underwent four rounds of treatment with increasing doses of an adenoviral vector encoding TK enzyme and GCV. Surviving cells were termed NP-18AR and displayed decreased sensitivity to treatment. This experiment analyses the transcriptomic effect of TK/GCV treatment on NP-18AR as compared to that of NP-18 cells.
2010-07-16 | GSE17137 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to evaluate the gene expression of M2-polarized bone marrow-derived macrophages (BMDM) compared with M0-BMDMs from wild type (WT) mouse. Methods: BMDMs were obtained from WT mice and polarized toward M2-BMDMs using IL-4 and M-CSF. M0-BMDMs were maintained in culture with M-CSF only. Total RNA of M2- and M0-BMDMs was extracted. BMDM RNA profiles were generated by deep sequencing for two groups (M2- versus M0-BMDM) with three mouse samples each. Results: There were significant differences between M2- and M0-BMDMs. Conclusions: Polarization of BMDMs from M0 to M2 induces various changes at the transcription level.
2024-03-31 | GSE183074 | GEO
Project description:We developed a high-throughput mutagenesis screen to comprehensively identify the cis-regulatory elements that control a target splicing event from the MST1R gene that codes for the RON receptor tyrosine kinase. Skipping of alternative exon 11 results in a constitutively active isoform that promotes epithelial to mesenchymal transition and thereby contributes to the invasive phenotype of tumors. We identified the RNA binding protein hnRNP H as an important regulator of RON exon 11 splicing. To map hnRNP H binding sites on the RON minigene with either wildtype or hnRNP H binding site mutant background, we performed hnRNP H iCLIP with RON wildtype or mutant minigene transfected HEK293T cells. iCLIP was performed according to a previously published protocol (PMID: 26463384). The iCLIP libraries were made from two (G331C and G348C) or three replicates (wildtype and G305A) of HEK293T cells at 24 h after RON minigene transfection. The cells were irradiated with 150 mJ/cm2 UV light at 254 nm. For the immunoprecipitation step, we used 7.5 µg of a polyclonal rabbit anti-HNRNPH antibody from Abcam (AB10374). RNase digestion was performed by adding 10 µl of 1/100 diluted RNase I (Ambion) to each sample. We performed the sequencing on an Illumina MiSeq or NextSeq500 with 75-nt single-end reads.
2018-06-27 | E-MTAB-6221 | biostudies-arrayexpress
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2008-12-20 | GSE12414 | GEO
Project description:The purpose of this experiment was to examine the differential transcriptional profiles of Caulobacter CB15N grown in M2-Glucose versus M2-Inositol. mRNA expression was compared between Caulobacter CB15N cells grown in M2-Glucose vs. M2-Inositol. Four arrays were run, two of each dye combination.
2010-06-30 | E-GEOD-12414 | biostudies-arrayexpress
Project description:Metastasis is the major cause of death in cancer patients, yet the genetic/epigenetic programs that drive metastasis are poorly understood. Here, we report a novel epigenetic reprogramming pathway that is required for breast cancer metastasis. Concerted differential DNA methylation is initiated by activation of the RON receptor tyrosine kinase by its ligand, macrophage stimulating protein (MSP). Through PI3K signaling, RON/MSP promotes expression of the G:T mismatch-specific thymine glycosylase MBD4. RON/MSP and MBD4-dependent aberrant DNA methylation results in misregulation of a specific set of genes. Knockdown of MBD4 reverses methylation at these specific loci, and blocks metastasis. We also show that the MBD4 glycosylase catalytic residue is required for RON/MSP-driven metastasis. Analysis of human breast cancers using a set of specific genes that are regulated by RON/MSP through MBD4-directed aberrant DNA methylation revealed that this epigenetic program is significantly associated with poor clinical outcome. Furthermore, inhibition of Ron kinase activity with a new pharmacological agent prevents activation of the RON/MBD4 pathway and blocks metastasis of patient-derived breast tumor grafts in vivo.
2014-01-02 | GSE52688 | GEO
Project description:Metastasis is the major cause of death in cancer patients, yet the genetic/epigenetic programs that drive metastasis are poorly understood. Here, we report a novel epigenetic reprogramming pathway that is required for breast cancer metastasis. Concerted differential DNA methylation is initiated by activation of the RON receptor tyrosine kinase by its ligand, macrophage stimulating protein (MSP). Through PI3K signaling, RON/MSP promotes expression of the G:T mismatch-specific thymine glycosylase MBD4. RON/MSP and MBD4-dependent aberrant DNA methylation results in misregulation of a specific set of genes. Knockdown of MBD4 reverses methylation at these specific loci, and blocks metastasis. We also show that the MBD4 glycosylase catalytic residue is required for RON/MSP-driven metastasis. Analysis of human breast cancers using a set of specific genes that are regulated by RON/MSP through MBD4-directed aberrant DNA methylation revealed that this epigenetic program is significantly associated with poor clinical outcome. Furthermore, inhibition of Ron kinase activity with a new pharmacological agent prevents activation of the RON/MBD4 pathway and blocks metastasis of patient-derived breast tumor grafts in vivo.
2014-01-02 | GSE52687 | GEO
Project description:Tachykinins (TKs) and their receptors have been shown to be expressed in the mammalian ovary. However, the biological roles for ovarian TKs have yet to be verified. Ci-TK and Ci-TK-R, characterized from the protochordate (ascidian), Ciona intestinalis, are prototypes of vertebrate TKs and their receptors. In the present study, we show a novel biological function of TKs as an inducible factor for oocyte growth using C. intestinalis as a model animal. Immunostaining demonstrated the specific expression of Ci-TK-R in test cells residing in oocytes at the vitellogenic stage. DNA microarray and real-time PCR substantiated that Ci-TK induced gene expression of several proteases including cathepsin D, chymotrypsin, and carboxypeptidase B2 and functionally unidentified lectins or glycosidases in the ovary. The enzymatic activities of the above proteases in the ovary were also shown to be enhanced by Ci-TK. Of particular significance is that treatment of Ciona oocytes with Ci-TK resulted in progression of growth from the vitellogenic stage to the post-vitellogenic stage, which was completely blocked by a TK antagonist or protease inhibitors. These results led to the conclusion that Ci-TK enhances growth of the vitellogenic oocytes via up-regulation of gene expression and enzymatic activities of the proteases. Keywords: tachykinins, ovary
2008-08-19 | GSE8821 | GEO