ArticleCarcinogenesis2010
Endoglin phosphorylation by ALK2 contributes to the regulation of prostate cancer cell migration.
Article in Carcinogenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Endoglin as a predictive biomarker for pemetrexed sensitivity in non-small-cell lung cancer: a cellular study.Cancer chemotherapy and pharmacology · 2025Article
- Correlation Between Endoglin and Malignant Phenotype in Human Melanoma Cells: Analysis of hsa-mir-214 and hsa-mir-370 in Cells and Their Extracellular Vesicles.Advances in experimental medicine and biology · 2023Article
- The role of endoglin and its soluble form in pathogenesis of preeclampsia.Molecular and cellular biochemistry · 2022Review
- Inhibition of Janus Kinase 1 synergizes docetaxel sensitivity in prostate cancer cells.Journal of cellular and molecular medicine · 2021Article
- Endoglin in the Spotlight to Treat Cancer.International journal of molecular sciences · 2021Review
- ACVR1 Function in Health and Disease.Cells · 2019Review
- Opposing roles and potential antagonistic mechanism between TGF-β and BMP pathways: Implications for cancer progression.EBioMedicine · 2019Review
- Article
- Small bowel adenocarcinoma arising in a patient with hereditary hemorrhagic telangiectasia: A case report.Oncology letters · 2016Article
- PRH/HHex inhibits the migration of breast and prostate epithelial cells through direct transcriptional regulation of Endoglin.Oncogene · 2014Article
- TGF-β cascade regulation by PPP1 and its interactors -impact on prostate cancer development and therapy.Journal of cellular and molecular medicine · 2014Review
- Improved survival outcomes in cancer patients with hereditary hemorrhagic telangiectasia.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2014Article
- Endoglin involvement in integrin-mediated cell adhesion as a putative pathogenic mechanism in hereditary hemorrhagic telangiectasia type 1 (HHT1).Frontiers in genetics · 2014Review
- Prostate cancer: the need for biomarkers and new therapeutic targets.Journal of Zhejiang University. Science. B · 2014Review
- Endoglin-mediated suppression of prostate cancer invasion is regulated by activin and bone morphogenetic protein type II receptors.PloS one · 2013Article
- Article
- Article
- Endoglin regulates cancer-stromal cell interactions in prostate tumors.Cancer research · 2011Article
- Endoglin expression in breast tumor cells suppresses invasion and metastasis and correlates with improved clinical outcome.Oncogene · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Endoglin, a transmembrane glycoprotein that acts as a transforming growth factor-beta (TGF-beta) coreceptor, is downregulated in PC3-M metastatic prostate cancer cells. When restored, endoglin expression in PC3-M cells inhibits cell migration in vitro and attenuates the tumorigenicity of PC3-M cells in SCID mice, though the mechanism of endoglin regulation of migration in prostate cancer cells is not known. The current study indicates that endoglin is phosphorylated on cytosolic domain threonine residues by the TGF-beta type I receptors ALK2 and ALK5 in prostate cancer cells. Importantly, in the presence of constitutively active ALK2, endoglin did not inhibit cell migration, suggesting that endoglin phosphorylation regulated PC3-M cell migration. Therefore, our results suggest that endoglin phosphorylation is a mechanism with relevant functional consequences in prostate cancer cells. These data demonstrate for the first time that TGF-beta receptor-mediated phosphorylation of endoglin is a Smad-independent mechanism involved in the regulation of prostate cancer cell migration.
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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.