ArticleClinical cancer research : an official journal of the American Association for Cancer Research2009
Sp-1 and c-Myc mediate lysophosphatidic acid-induced expression of vascular endothelial growth factor in ovarian cancer cells via a hypoxia-inducible factor-1-independent mechanism.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 60 citations in OpenAlex.
- Inflammatory milieu and role of epigenetic modifications in high-grade serous ovarian cancer.Clinical epigenetics · 2026Review
- Deficiency of lysophosphatidic acid receptor 3 decreases erythropoietin production in hypoxic mouse kidneys.Lipids in health and disease · 2024Article
- Friend and foe: the regulation network of ascites components in ovarian cancer progression.Journal of cell communication and signaling · 2023Review
- The lysophosphatidic acid-regulated signal transduction network in ovarian cancer cells and its role in actomyosin dynamics, cell migration and entosis.Theranostics · 2023Article
- Review
- Lysophosphatidic acid induces tumor necrosis factor-alpha to regulate a pro-inflammatory cytokine network in ovarian cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Article
- β‑elemene inhibits the generation of peritoneum effusion in pancreatic cancer via suppression of the HIF1A‑VEGFA pathway based on network pharmacology.Oncology reports · 2019Article
- Review
- Rho-Associated Coiled-Coil Kinase (ROCK) in Molecular Regulation of Angiogenesis.Theranostics · 2018Review
- G Protein-Coupled Receptors at the Crossroad between Physiologic and Pathologic Angiogenesis: Old Paradigms and Emerging Concepts.International journal of molecular sciences · 2017Review
- Effect of ART1 on the proliferation and migration of mouse colon carcinoma CT26 cells in vivo.Molecular medicine reports · 2017Article
- The Unique Molecular and Cellular Microenvironment of Ovarian Cancer.Frontiers in oncology · 2017Review
- Role of lipid phosphate phosphatase 3 in human aortic endothelial cell function.Cardiovascular research · 2016Article
- Article
- Lysophosphatidic Acid Up-Regulates Hexokinase II and Glycolysis to Promote Proliferation of Ovarian Cancer Cells.Neoplasia (New York, N.Y.) · 2015Article
- Diagnostic and prognostic significance of lysophosphatidic acid in malignant pleural effusions.Journal of thoracic disease · 2014Article
- Transcriptional regulation prediction of antiestrogen resistance in breast cancer based on RNA polymerase II binding data.BMC bioinformatics · 2014Article
- Loss of epigenetic Kruppel-like factor 4 histone deacetylase (KLF-4-HDAC)-mediated transcriptional suppression is crucial in increasing vascular endothelial growth factor (VEGF) expression in breast cancer.The Journal of biological chemistry · 2013Article
- Aberrant lipid metabolism: an emerging diagnostic and therapeutic target in ovarian cancer.International journal of molecular sciences · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
purposeLysophosphatidic acid (LPA), which is present in ascites of ovarian cancer patients, stimulates expression of vascular endothelial growth factor (VEGF). VEGF is essential for the development and abdominal dissemination of ovarian cancer. We examined how LPA drives VEGF expression to gain a better understanding of tumor angiogenesis under normoxic conditions. EXPERIMENTAL
designELISA, Northern blotting, immunoblotting, quantitative PCR, and promoter reporter analysis in combination with small interfering RNA and pharmacologic inhibitors were used to examine LPA-induced VEGF expression and the underlying mechanisms.
resultsLPA stimulated expression of multiple VEGF variants. A 123-bp fragment proximal to the transcriptional initiation site was identified to be functional promoter region responsible for the response to LPA. The fragment harbors consensus sites for several transcription factors including c-Myc and Sp-1 but not hypoxia-inducible factor-1. Blockade of Rho, ROCK, or c-Myc reduced LPA-dependent VEGF production and promoter activation, suggesting that the G12/13-Rho-ROCK-c-Myc cascade partially contributes to VEGF induction by LPA. More significantly, the multiple Sp-1 sites within the responsive region of the VEGF promoter were essential for LPA-mediated transcription. LPA induced Sp-1 phosphorylation and DNA-binding and transcriptional activities. The silencing of Sp-1 expression with small interfering RNA or inhibition of Sp-1 with pharmacologic inhibitors blocked VEGF production induced by LPA.
conclusionsLPA stimulates hypoxia-inducible factor-1-independent VEGF expression to promote tumor angiogenesis through activation of the c-Myc and Sp-1 transcription factors.
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