Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA116489 | ENA |
REPOSITORIES: ENA
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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
| PRJNA136785 | ENA
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
| PRJNA108305 | ENA
Project description:Activated HER2 and EGFR stimulate the Ras small GTPases, which in turn primarily activate the MAPK, PI3K-Akt and RalGEF-Ral pathways. While activation of the MAPK and PI3K-Akt pathways downstream of HER2 and EGFR promote mammary tumorigenesis, little is known regarding the role of the RalGEF-Ral pathway. RalGEFs convert the small GTPases RalA and RalB to an active GTP-bound state. Of the two proteins, only activated RalA is transforming, while RalB is more important for cell motility, and hence we investigated the role of RalA in HER2-overexpressing and EGFR-positive breast cancer. We now report that shRNA-mediated knockdown of RalA reduced the in vitro transformed growth and in vivo tumorigenic growth of MDA-MB-231 human breast cancer cells, while knockdown of RalB reduced migration and invasion. Lastly, we demonstrate that expression of activated HER2 increases RalA-GTP levels, and that a number of genes associated with activated RalA are elevated in tumor compared to normal mammary tissue. Taken together, these results suggest a possible role for RalA in mammary tumorigenesis. Four independent cultures of HEK-HT cells stably infected with a retrovirus confirmed to expressed RalAQ72L and four independent cultures of HEK-HT cells stably infected with a control retrovirus RalA activation expression analysis
2016-02-13 | E-GEOD-19295 | biostudies-arrayexpress
Project description:Brown adipose tissue (BAT) is a thermogenic organ that dissipates stored energy as heat to maintain body temperature in infants and small mammals. This process may also provide protection from development of diet-induced obesity. We found that the bioactive lipid mediator lysophosphatidic acid (LPA) markedly decreases differentiation of cultured primary brown adipocyte precursors, while potent selective inhibitors of the LPA-generating enzyme autotaxin (ATX) promote differentiation. Transgenic mice overexpressing ATX exhibited reduced expression of BAT-related genes in peripheral white adipose tissue and accumulated significantly more fat than wild-type controls when fed a high fat diet. Our results indicate that ATX and its product LPA are physiologically relevant negative regulators of brown fat adipogenesis and suggest that a decrease in peripheral brown adipose tissue results in increased susceptibility to diet-induced obesity in mice.
2011-06-01 | GSE26442 | GEO