ArticleCancer science2017
Vasohibin-2 is required for epithelial-mesenchymal transition of ovarian cancer cells by modulating transforming growth factor-β signaling.
Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- The Role of Cytokines in Epithelial-Mesenchymal Transition in Gynaecological Cancers: A Systematic Review.Cells · 2023Pooled it
- Prognostic, diagnostic and therapeutic value of the cancer tubulin code.Cancer metastasis reviews · 2026Review
- Peptide-based covalent inhibitor of tubulin detyrosination promotes mesenchymal-to-epithelial transition in lung cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- CILP attenuates pulmonary fibrosis through the TGF-β1/SMAD3 pathway.European journal of medical research · 2025Article
- KY216-tubulin complex captures VASH2 to inhibit NSCLC metastasis.Nature communications · 2025Article
- LINC00654 promotes ovarian cancer progression by facilitating nuclear export of HuR and stabilizing oncogenic mRNAs.Oncogene · 2025Article
- Review
- How does the tubulin code facilitate directed cell migration?Biochemical Society transactions · 2025Review
- A preliminary study on the mechanism of VASH2 in childhood medulloblastoma.Scientific reports · 2023Article
- Novel strategy of liver cancer treatment with modified antisense oligonucleotides targeting human vasohibin-2.Cancer science · 2023Article
- Microtubule detyrosination drives symmetry breaking to polarize cells for directed cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- [Vasohibin-2 promotes proliferation and metastasis of cervical cancer cells by regulating epithelial-mesenchymal transition].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Vasohibin 2 promotes lymphangiogenesis of lung squamous cell carcinoma through snail-dependent vascular endothelial growth factor-D (VEGF-D) signaling pathway.Annals of translational medicine · 2022Article
- Latency-associated Peptide Degradation Fragments Produced in Stellate Cells and Phagocytosed by Macrophages in Bile Duct-ligated Mouse Liver.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021Article
- Prognostic significance of vasohibin-1 and vasohibin-2 immunohistochemical expression in gastric cancer.Surgery today · 2020Article
- Plasma vasohibin-1 and vasohibin-2 are useful biomarkers in patients with esophageal squamous cell carcinoma.Esophagus : official journal of the Japan Esophageal Society · 2020Article
- Genetic Deletion of Vasohibin-2 Exacerbates Ischemia-Reperfusion-Induced Acute Kidney Injury.International journal of molecular sciences · 2020Article
- Targeting angiogenesis and lymphangiogenesis in kidney disease.Nature reviews. Nephrology · 2020Review
- Long noncoding RNA RBMS3-AS3 acts as a microRNA-4534 sponge to inhibit the progression of prostate cancer by upregulating VASH1.Gene therapy · 2020Article
- Role of VEGF-A and LRG1 in Abnormal Angiogenesis Associated With Diabetic Nephropathy.Frontiers in physiology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vasohibin-2 (VASH2) is a homolog of VASH1, an endothelium-derived angiogenesis inhibitor. Vasohibin-2 is mainly expressed in cancer cells, and has been implicated in the progression of cancer by inducing angiogenesis and tumor growth. Although VASH2 has been recently reported to be involved in epithelial-mesenchymal transition (EMT), its precise roles are obscure. The aim of the present study was to clarify the role of VASH2 in the EMT of cancer cells in relation to transforming growth factor-β (TGF-β) signaling, which is a major stimulator of EMT. Decreased expression of VASH2 in ovarian cancer cells significantly repressed the expression of TGF-β type I receptor, namely activin receptor-like kinase 5. Transforming growth factor-β1-induced phosphorylation of Smad2 and Smad3 was markedly decreased in VASH2 knockdown cells while the expression of Smad2 and Smad3 was unchanged. Accordingly, the responses to TGF-β1 shown by promoter assay and plasminogen activator inhibitor type 1 expression were significantly attenuated in VASH2 knockdown cells. Furthermore, knockdown of VASH2 in cancer cells abrogated the TGF-β1-induced reduced expression of epithelial markers including E-cadherin, and the elevated expression of mesenchymal markers including fibronectin, ZEB2, and Snail2, suggesting that endogenous VASH2 is required for TGF-β1-induced EMT. In accordance with these results, the effects of TGF-β1 on cell morphology, migration, invasion, and MMP2 expression were also abrogated when VASH2 was knocked down. These results indicate that VASH2 played a significant role in the EMT by modulating the TGF-β signaling. We propose that VASH2 would be a novel molecular target for the prevention of EMT in cancers.
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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.