Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA242799 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Lysophosphatidic acid (LPA) and LPA-receptor (LPAR)-activated G-protein alpha subunits encoded by GNAi2, GNA12, and GNA13 play a crucial role in ovarian cancer progression. While the general signaling mechanism regulated by LPA-LPAR-signaling had previously been characterized, the global transcriptomic network regulated by individual G protein alpha-subunits in ovarian cancer pathophysiology remains largely unknown. To define the specific oncogenic networks regulated by LPA-stimulated GNAi2, GNA12, and GNA13 in ovarian cancer, transcriptomic analyses were carried out using SKOV3 cells in which the expression of GNAi2, GNA12, or GNA134 was silenced in an Agilent SurePrint G3 Human Comparative Genomic Hybridization 8x60 microarray platform.
2021-08-25 | GSE173214 | GEO
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:We report that the lysophosphatidic acid receptor 4 (LPAR4) is specifically upregulated on cells exposed to environmental stress or cancer drugs where it promotes stress tolerance, self-renewal, and tumor initiation. We find that ectopic LPAR4-expressing tumors display an enrichment of key extracellular matrix (ECM)-related genes that are established drivers of cancer stemness, and surprisingly do not require stimulation with the canonical LPAR4 ligand, LPA. From this RNAseq data, we observed that LPAR4 promotes a subset of genes, mainly extracellular matrix related genes, independent of its ligand LPA in patient-derived xenograft cells.
2022-08-15 | GSE198002 | GEO
Project description:We report the differential gene expression patterns of TILs from two patients after treating the cells with lysophosphatidic acid (LPA) for 2 or 3 hours. Among the common LPA-regulated genes are transcription factors and other immediate early genes as well as T-cell regulatory cell-surface molecules
2023-01-15 | GSE143697 | GEO
Project description:Lysophosphatidic acid (LPA) is a bioactive lipid enriched in highly immunosuppressive neoplasms like ovarian cancer (OvCa). While LPA is known to enhance the tumorigenic capacity of malignant cells, the immunomodulatory role of this phospholipid in cancer remains largely unexplored. Here, we report that LPA operates as a negative regulator of type-I interferon (IFN) responses in OvCa. Ablation of the LPAgenerating enzyme autotaxin in OvCa cells reprogrammed the tumor immune microenvironment, extended host survival, and improved the effects of therapies that elicit protective responses driven by type-I IFN. Mechanistically, LPA sensing by dendritic cells triggered PGE2 synthesis that suppressed type-I IFN signaling via autocrine EP4 engagement. Moreover, we identified an LPA-controlled, immune-derived gene signature associated with weak responses to combined PARP inhibition and PD-1 blockade in OvCa patients. Controlling LPA production or sensing in tumors may therefore be useful to improve cancer immunotherapies that rely on robust induction of type-I IFN.
2022-08-02 | GSE182062 | GEO
Project description:Human gingival fibroblasts: control vs. lysophosphatidic acid (LPA 18:1)-treated
| PRJNA246749 | ENA
Project description:LPA is a natural bioactive lipid with growth factor-like functions due to activation of series of six G protein-coupled receptors (LPA1-6). In this study we determine the LPA induced early-miRNA expression profile in human breast cancer cell lines MDA-MB-231
2015-05-05 | GSE64100 | 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:Pluripotent stem cells can be maintained in a continuum of cellular states with distinct features. Exogenous lipid supplements are commonly utilized to shift the balance of global metabolism relieving the dependence on de novo lipogenesis. However, it is largely unexplored how specific lipid components regulate metabolism and pluripotency state. In this study, we investigate the impact of lipid supplements on human embryonic stem cells (hESCs), and report that signaling lipid lysophosphatidic acid (LPA) is the key component to shift the metabolic landscape in lipid supplement AlbuMAX. Although the maintenance of ERK phosphorylation and primed pluripotency is independent of exogenous lipids, LPA increases ERK phosphorylation, especially upon niche disintegration. We further demonstrate that LPA leads to distinctive transcriptome profile that is not associated with de novo lipogenesis. We also show that LPA causes unique and reversible phenotypes in cell cycle, morphology and mitochondria. This study reveals an LPA -induced primed state that allow people to drastically alter cell physiology for basic research and stem cell applications with hESCs.
2021-11-16 | GSE165892 | GEO
Project description:Pluripotent stem cells can be maintained in a continuum of cellular states with distinct features. Exogenous lipid supplements are commonly utilized to shift the balance of global metabolism relieving the dependence on de novo lipogenesis. However, it is largely unexplored how specific lipid components regulate metabolism and pluripotency state. In this study, we investigate the impact of lipid supplements on human embryonic stem cells (hESCs), and report that signaling lipid lysophosphatidic acid (LPA) is the key component to shift the metabolic landscape in lipid supplement AlbuMAX. Although the maintenance of ERK phosphorylation and primed pluripotency is independent of exogenous lipids, LPA increases ERK phosphorylation, especially upon niche disintegration. We further demonstrate that LPA leads to distinctive transcriptome profile that is not associated with de novo lipogenesis. We also show that LPA causes unique and reversible phenotypes in cell cycle, morphology and mitochondria. This study reveals an LPA -induced primed state that allow people to drastically alter cell physiology for basic research and stem cell applications with hESCs.
2022-03-08 | GSE198007 | GEO