ArticleMolecular cancer2012
Hypoxia and estrogen are functionally equivalent in breast cancer-endothelial cell interdependence.
Article in Molecular cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 47 citations in OpenAlex.
- Sexual dimorphism in cancer: molecular mechanisms and precision oncology perspectives.Biology of sex differences · 2026Review
- Leveraging hypoxia-related genes signature for predicting the prognosis of bladder cancer.Translational andrology and urology · 2025Article
- Understanding the role of TNFR2 signaling in the tumor microenvironment of breast cancer.Journal of experimental & clinical cancer research : CR · 2024Review
- Activation of the hypoxia response in the aging cerebrovasculature protects males against cognitive impairment.Aging cell · 2024Article
- Searching for LINCS to Stress: Using Text Mining to Automate Reference Chemical Curation.Chemical research in toxicology · 2024Article
- Obesity and leptin in breast cancer angiogenesis.Frontiers in endocrinology · 2024Review
- Nogo-B receptor increases glycolysis and the paclitaxel resistance of estrogen receptor-positive breast cancer via the HIF-1α-dependent pathway.Cancer gene therapy · 2023Article
- Obesity as a Risk Factor for Breast Cancer-The Role of miRNA.International journal of molecular sciences · 2022Review
- Transgenic construction and functional miRNA analysis identify the role of miR-7 in prostate cancer suppression.Oncogene · 2022Article
- Present Status, Challenges, and Prospects of Dihydromyricetin in the Battle against Cancer.Cancers · 2022Review
- Multifaceted Interplay between Hormones, Growth Factors and Hypoxia in the Tumor Microenvironment.Cancers · 2022Review
- Nuclear Receptor-Mediated Metabolic Reprogramming and the Impact on HR+ Breast Cancer.Cancers · 2021Review
- Regulatory Network Analysis in Estradiol-Treated Human Endothelial Cells.International journal of molecular sciences · 2021Article
- Role of FSH and FSH receptor on HUVECs migration.Gene therapy · 2021Article
- Distinct JNK/VEGFR signaling on angiogenesis of breast cancer-associated pleural fluid based on hormone receptor status.Cancer science · 2021Article
- The Mechanism of Warburg Effect-Induced Chemoresistance in Cancer.Frontiers in oncology · 2021Review
- Reprogramming of Mesothelial-Mesenchymal Transition in Chronic Peritoneal Diseases by Estrogen Receptor Modulation and TGF-β1 Inhibition.International journal of molecular sciences · 2020Review
- Role of TXNDC5 in tumorigenesis of colorectal cancer cells: In vivo and in vitro evidence.International journal of molecular medicine · 2018Article
- Crosstalk between Notch, HIF-1α and GPER in Breast Cancer EMT.International journal of molecular sciences · 2018Review
- Macrophage inflammatory factors promote epithelial-mesenchymal transition in breast cancer.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundRapid breast tumor development relies on formation of new vasculature to supply the growing malignancy with oxygenated blood. Previously we found that estrogen aided in this neovasculogenesis via recruitment of bone marrow derived endothelial progenitor cells (BM-EPCs), leading to increased vessel formation and vascular endothelial growth factor (VEGF) production in vivo. However, the cellular mechanism of this induction and the signaling pathways involved need elucidation.
resultsUsing the murine mammary cell line TG1-1 we observed estrogen (E2) lead to an up regulation of hypoxia inducible factor-1 (HIF-1), an effect abrogated by the anti-estrogen Fulvestrant and the HIF-1 inhibitor YC-1 (3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole) suggesting the interchangeability of hypoxia and estrogen mediated effects. Estrogen modulation of HIF-1 and subsequent effects on endothelial cells is dependent on the Akt/PI3K pathway and protein synthesis as validated by the use of the inhibitors wortmannin and cycloheximide which abrogated estrogen's effects respectively. Estrogen treated TG1-1 cells secreted higher levels of VEGF which were comparable to secreted levels from cells grown under hypoxic conditions. Soluble factors in conditioned media from E2 treated breast cancer cells also lead to migration and tube formation of human umbilical vein endothelial cells (HUVEC) in vitro.
conclusionsOur data provide evidence that estrogen signaling mediates the tumor vasculogenic process required for breast cancer progression and involves a key regulator of the hypoxia signaling pathway. Further, hypoxia and estrogen are interchangeable as both similarly modulate epithelial-endothelial cell interaction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.