Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA116489 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Lysophosphatidic acid (LPA) acts through high-affinity G protein-coupled receptors to mediate a plethora of physiological and pathological activities associated with tumorigenesis. LPA receptors and autotaxin (ATX/LysoPLD), the primary enzyme producing LPA, are aberrantly expressed in multiple cancer lineages. However, the role of ATX and LPA receptors in the initiation and progression of breast cancer has not been evaluated. We demonstrate that expression of ATX or each edg family LPA receptor in mammary epithelium of transgenic mice is sufficient to induce a high frequency of late-onset, estrogen receptor (ER)-positive, invasive, and metastatic mammary cancer. Thus, ATX and LPA receptors can contribute to the initiation and progression of breast cancer.
2009-06-11 | GSE15263 | GEO
Project description:LPAR1 (lysophosphatidic acid receptor 1) is identified in targeted siRNA screens which is required for the survival and maintenance of nueral crest stem cells (NCSC) as well as the growth and invasion of melanoma cells. To gain mechanistic insights into how LPAR signaling modulates melanoma cell growth, We conducted an Illumina genome-wide gene expression microarray experiment to profile melanoma cells treated with the autotaxin inhibitor, HA130. Melanoma cells treated with vehicle control,DMSO is included as a control.
2017-12-01 | GSE92764 | GEO
Project description:Autotaxin (ATX, Enpp2) is a secreted lysophospholipase D catalyzing the production of lysophosphatidic acid (LPA), a pleiotropic growth factor-like phospholipid. Upregulated ATX expression has been detected in various chronic inflammatory disorders and different types of cancer; among them increased ATX mRNA or immunohistochemical staining has been suggested in Hepatocellular carcinoma (HCC) patients. Conditional deletion of ATX/Enpp2 specifically from hepatocytes, in AlbEnpp2-/- mice, attenuated the DEN/CCl4-mediated HCC development in mice. To obtain mechanistic insights into the mode of action of the ATX/LPA axis in HCC development, we performed whole liver, genome wide expression profiling of DEN/CCl4-induced HCC upon the genetic deletion of Autotaxin (ATX) in AlbEnpp2-/- mice in comparison with DEN/CCl4-treated and untreated wt littermate mice.
2016-11-30 | E-MTAB-4648 | biostudies-arrayexpress
Project description:Autotaxin and its product lysophosphatidic acid suppress brown adipose differentiation and promote diet-induced obesity in mice
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Project description:Gene expression profiling of samples from normal virgin mammary glands, hyperplastic mammary glands, mamary tumors, and lung metastases from MMTV-Wnt-1 transgenic (TG) mice, and mammary tumors and lung metastases from MMTV-Neu trangenic (TG) mice Keywords: Array analysis, multi-step tumorigenesis, metastasis, MMTV-Wnt-1 trangenic mice, MMTV-Neu transgenic mice
2005-09-30 | GSE2860 | GEO
Project description:Autotaxin (ATX), encoded by ENPP2, catalyzes the production of lysophosphatidic acid (LPA), an important regulator within the tumor microenvironment (TME). ATX is a clinical target in pancreatic ductal adenocarcinoma (PDAC), yet the pro-tumorigenic action of the ATX/LPA axis in PDAC remains unclear. PDAC is characterized by a highly fibrotic tumor microenvironment (TME) due to an abundance of cancer associated fibroblasts (CAFs), acting as a barrier to therapy and contributing to the poor survival of PDAC patients. The mechanism by which ATX inhibition influences CAFs and their secretome is still not fully characterized. To identified potential downstream mediators of ATX signaling, we performed RNA-seq of pancreatic CAF-derived cell line 0082T treated with Autotaxin inhibitors, IOA-289 and PF-8380. PF-8380 treatment resulted in a higher number of differentially expressed genes compared to IOA-289 treatment. IOA-289 treatment resulted in only four significantly differentially expressed genes (CTGF, PLIN2, HHIP, and AHNAK). However, only PLIN2, which was upregulated and CTGF, which was downregulated, overlapped between the two ATX inhibitors. As CTGF (connective tissue growth factor) is a pro-fibrotic and pro-tumorigenic factor, it suggests a key role for CAF-derived ATX in promoting autocrine and paracrine pro-tumorigenic signaling in PDAC.
2024-10-06 | E-MTAB-14494 | biostudies-arrayexpress
Project description:Conjugated linoleic acid suppresses FAS and promotes mammary tumorigenesis in PyV-MT mice
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Project description:We investigated whether vascular basement membrane (BM) laminins influence vascular zonation by performing single-cell RNA sequencing (scRNAseq) on cerebral blood vessels from Lama4-/- mice - lacking the major vascular laminin 4 in endothelial and smooth muscle BMs - and wild-type littermates. Our dataset expands existing cerebral vascular transcriptomic profiles and reveals that Lama4-/- endothelial cells exhibit increased arterial marker expression and reduced postcapillary venule identity. In vitro and in vivo studies indicate that compensatory upregulation of laminin 5 in Lama4-/- vessels enhances expression of junctional proteins (Ocln, Cldn5) and promotes vessel contractility via increased expression of contractile genes in pericytes, which reside within the endothelial BM. Additionally, loss of Lama4 upregulates expression of large artery markers (Gja4, Dll4, Edn1,Tgfb2) and resulted in elevated autotaxin (Enpp2) levels, a key enzyme in lysophosphatidic acid production implicated in stroke. Accordingly, Lama4-/- mice exhibit worsened stroke outcomes, driven not by immune infiltration or junctional defects, but by increased vascular permeability likely mediated by autotaxin and/or activation of resident myeloid cells. Our data suggest that laminin 4/5 ratios in vascular BMs regulate functional zonation between arterioles, capillaries and postcapillary venules by modulating metabolic pathways in endothelial and mural cells, and indirectly influencing resident myeloid cells.
2026-02-25 | GSE308748 | GEO
Project description:We investigated whether vascular basement membrane (BM) laminins influence vascular zonation by performing single-cell RNA sequencing (scRNAseq) on cerebral blood vessels from Lama4-/- mice - lacking the major vascular laminin 4 in endothelial and smooth muscle BMs - and wild-type littermates. Our dataset expands existing cerebral vascular transcriptomic profiles and reveals that Lama4-/- endothelial cells exhibit increased arterial marker expression and reduced postcapillary venule identity. In vitro and in vivo studies indicate that compensatory upregulation of laminin 5 in Lama4-/- vessels enhances expression of junctional proteins (Ocln, Cldn5) and promotes vessel contractility via increased expression of contractile genes in pericytes, which reside within the endothelial BM. Additionally, loss of Lama4 upregulates expression of large artery markers (Gja4, Dll4, Edn1,Tgfb2) and resulted in elevated autotaxin (Enpp2) levels, a key enzyme in lysophosphatidic acid production implicated in stroke. Accordingly, Lama4-/- mice exhibit worsened stroke outcomes, driven not by immune infiltration or junctional defects, but by increased vascular permeability likely mediated by autotaxin and/or activation of resident myeloid cells. Our data suggest that laminin 4/5 ratios in vascular BMs regulate functional zonation between arterioles, capillaries and postcapillary venules by modulating metabolic pathways in endothelial and mural cells, and indirectly influencing resident myeloid cells.
2026-02-25 | GSE309181 | GEO