ArticleNeoplasia (New York, N.Y.)2005
Endothelin-1 inhibits apoptosis in prostate cancer.
Article in Neoplasia (New York, N.Y.), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 102 citations in OpenAlex.
- Humoral Immune Response against Nontargeted Tumor Antigens after Treatment with Sipuleucel-T and Its Association with Improved Clinical Outcome.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Trial
- Endothelin and the tumor microenvironment: a finger in every pie.Clinical science (London, England : 1979) · 2024Review
- Immunological facets of prostate cancer and the potential of immune checkpoint inhibition in disease management.Theranostics · 2024Review
- The Potential Biotherapeutic Targets of Contrast-Induced Acute Kidney Injury.International journal of molecular sciences · 2023Review
- The EDN1/EDNRA/β‑arrestin axis promotes colorectal cancer progression by regulating STAT3 phosphorylation.International journal of oncology · 2023Article
- The adaptation model of immunity: Is the goal of central tolerance to eliminate defective T cells or self-reactive T cells?Scandinavian journal of immunology · 2022Article
- The role of tumor microenvironment and exosomes in dormancy and relapse.Seminars in cancer biology · 2022Review
- A network map of endothelin mediated signaling pathway.Journal of cell communication and signaling · 2021Article
- Inhibition of endothelin-B receptor signaling synergizes with MAPK pathway inhibitors in BRAF mutated melanoma.Oncogene · 2021Article
- Putting the Pieces Together: Completing the Mechanism of Action Jigsaw for Sipuleucel-T.Journal of the National Cancer Institute · 2020Review
- Review
- Molecular mechanisms and clinical management of cancer bone metastasis.Bone research · 2020Review
- Human Cardiac Progenitor Cells Enhance Exosome Release and Promote Angiogenesis Under Physoxia.Frontiers in cell and developmental biology · 2020Article
- Endothelin-1 Augments Therapeutic Potency of Human Mesenchymal Stem Cells via CDH2 and VEGF Signaling.Molecular therapy. Methods & clinical development · 2019Article
- EAF2 and p53 Co-Regulate STAT3 Activation in Prostate Cancer.Neoplasia (New York, N.Y.) · 2018Article
- Article
- Cytoprotective effect of neuropeptides on cancer stem cells: vasoactive intestinal peptide-induced antiapoptotic signaling.Cell death & disease · 2017Article
- Functions of endothelin-1 in apoptosis and migration in hepatocellular carcinoma.Experimental and therapeutic medicine · 2017Article
- Endothelin-1 Expression in Prostate Needle Biopsy Specimens Correlated With Aggressiveness of Prostatic Cancer.Iranian journal of pathology · 2017Article
- Endothelin-1 (ET-1) induces resistance to bortezomib in human multiple myeloma cells via a pathway involving the ETB receptor and upregulation of proteasomal activity.Journal of cancer research and clinical oncology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelin-1 (ET-1), produced by the prostate epithelia, likely plays an important role in the progression of prostate cancer. ET-1 can bind two receptor subtypes; generally, binding of the endothelin receptor A (ET(A)) induces a survival pathway, whereas binding of the endothelin receptor B (ET(B)) mediates clearance of circulating ET-1 as well as promotes apoptosis. In prostate carcinoma, hypermethylation of the ET(B) promoter results in repression of ET(B) expression, thereby eliminating the negative growth response that ET-1 binding elicits through this receptor. Therefore, activation of ET(A) exclusively provides a pathway for survival advantage. Our current studies examine the mechanisms by which activation of the ET(A) may allow growth/survival. ET-1 treatment of prostate tumor cells significantly decreased paclitaxel-induced apoptosis through activation of the ET(A) subtype. The anti-apoptotic effects of ET-1 are mediated, at least in part, through the Bcl-2 family. Although no significant changes in Bcl-2 expression occurred with ET-1 treatment, the pro-apoptotic family members Bad, Bax, and Bak all decreased significantly. Further analysis of the survival pathway demonstrated that phosphorylation of Akt occurs with ET-1 treatment in a time- and dose-dependent manner through phosphatidyinositol 3-kinase activation. These data support the combination of ET(A) antagonists and apoptosis-inducing therapies for prostate cancer treatment.
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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.