ArticleJournal of cancer research and clinical oncology2021
Ephrin-A2 promotes prostate cancer metastasis by enhancing angiogenesis and promoting EMT.
Article in Journal of cancer research and clinical oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 59 citations in OpenAlex.
- Transcriptional activation of EPHB1 by SOX2 promotes epithelial-mesenchymal transition and metastasis in esophageal squamous cell carcinoma.Clinical & experimental metastasis · 2026Article
- Osteocyte-Derived GDF15 Promotes Paclitaxel Resistance, Tumor Growth, and Bone Microenvironment Regulation in Prostate Cancer.Current issues in molecular biology · 2026Article
- The FOSB-IGFBP5-IGF-1 axis: a novel regulatory pathway that suppresses prostate cancer growth.Cancer gene therapy · 2026Article
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- PEAK1 promotes prostate cancer progression and docetaxel resistance by mediating the polarization of tumor-associated macrophages.European journal of medical research · 2026Article
- EMT and cancer stem cells: Drivers of therapy resistance and promising therapeutic targets.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2025Review
- EphrinA2 promotes glioma cell migration and invasion through EphA2 and FAK.Cancer cell international · 2025Article
- Matrix metalloproteinase-driven epithelial-mesenchymal transition: implications in health and disease.Journal of translational medicine · 2025Review
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- Transcriptomic analysis reveals a critical role for activating GScientific reports · 2024Article
- Tight Junctions and Cancer: Targeting Claudin-1 and Claudin-4 in Thyroid Pathologies.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Identification of metastasis-related genes for predicting prostate cancer diagnosis, metastasis and immunotherapy drug candidates using machine learning approaches.Biology direct · 2024Article
- Differential analysis of histopathological and genetic markers of cancer aggressiveness, and survival difference in EBV-positive and EBV-negative prostate carcinoma.Scientific reports · 2024Article
- Upregulation of SEMP1 Contributes to Improving the Biological Functions of Trophoblast via the PI3K/AKT Pathway in Preeclampsia.Molecular biotechnology · 2024Article
- Possible prognostic impact of PKCι genetic variants in prostate cancer.Cancer cell international · 2024Article
- Evaluating the predictive value of angiogenesis-related genes for prognosis and immunotherapy response in prostate adenocarcinoma using machine learning and experimental approaches.Frontiers in immunology · 2024Article
- Anoikis in prostate cancer bone metastasis gene signatures and therapeutic implications.Frontiers in oncology · 2024Article
- Aptamers as Potential Therapeutic Tools for Ovarian Cancer: Advancements and Challenges.Cancers · 2023Review
- Transcriptome Analysis of the Inhibitory Effects of 20(S)-Protopanaxadiol on NCI-H1299 Non-Small Cell Lung Cancer Cells.Molecules (Basel, Switzerland) · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEphrin-A2, a member of the Eph receptor subgroup, is used in diagnosing and determining the prognosis of prostate cancer. However, the role of ephrin-A2 in prostate cancer is remains elusive.
methodsWe established stable clones overexpressing or silencing ephrin-A2 from prostate cancer cells. Then, CCK-8 was used in analyzing the proliferation ability of cells. CD31 staining was used in evaluating angiogenesis. Migration and invasion assay were conducted in vivo and in vitro. The expression of EMT-related markers was evaluated in prostate cancer cells through Western blotting.
resultsWe revealed that the ectopic expression of ephrin-A2 in prostate cancer cells facilitated cell migration and invasion in vitro and promoted tumor metastasis and angiogenesis in vivo and that the silencing of ephrin-A2 completely reversed this effect. Although ephrin-A2 did not affect tumor cell proliferation in vitro, ephrin-A2 significantly promoted primary tumor growth in vivo. Furthermore, to determine the biological function of ephrin-A2, we assayed the expression of EMT-related markers in stable-established cell lines. Results showed that the overexpression of ephrin-A2 in prostate cancer cells down-regulated the expression of epithelial markers (ZO-1, E-cadherin, and claudin-1) and up-regulated the expression of mesenchymal markers (N-cadherin, β-catenin, vimentin, Slug, and Snail), but the knocking out of ephrin-A2 opposed the effects on the expression of EMT markers.
conclusionsThese findings indicate that ephrin-A2 promotes prostate cancer metastasis by enhancing angiogenesis and promoting EMT and may be a potentially therapeutic target in metastatic prostate cancer.
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