ArticleCancer biology & therapy2017
Anti-angiogenic treatment promotes triple-negative breast cancer invasion via vasculogenic mimicry.
Article in Cancer biology & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 96 citations in OpenAlex.
- Targeting the tumor microenvironment: a new strategy for natural products in breast cancer therapy.Natural products and bioprospecting · 2026Review
- Framework for evaluating in vitro vasculogenic mimicry using structural and metabolic parameters.Cell reports methods · 2026Article
- Clinical utilities of platelet-derived growth factor signaling in breast cancer.Pharmacological research · 2026Review
- Axitinib promotes stemness and vasculogenic mimicry in triple-negative breast cancer by disrupting THBS1-CD47 axis-mediated endothelial-tumor cell communication.Apoptosis : an international journal on programmed cell death · 2026Article
- Vasculogenic mimicry and breast cancer prognosis: Insights into predictive model development.Oncology letters · 2026Article
- Preclinical Study of Radiolabeled LyP-1 for Detecting Sunitinib-induced Changes in the Tumor Microenvironment and Synergistic Antitumor Effects in Triple-negative Breast Cancer.Molecular imaging and biology · 2026Article
- Article
- 2'-Nitroflavone targets PARP1 and alters cytoskeleton to inhibit triple-negative breast cancer progression.Scientific reports · 2026Article
- The TRPM7 inhibitor carvacrol suppresses angiogenesis and vasculogenic mimicry in triple-negative breast cancer.International journal of biological sciences · 2026Article
- Emerging strategies for targeting vasculogenic mimicry in breast cancer treatment.Discover oncology · 2025Review
- Rhapontigenin Suppresses Leptin-Induced Vasculogenic Mimicry by Inhibiting STAT3-Aquaporin-1 Axis in TNBC Cells.Biomedicines · 2025Article
- Article
- Vasculogenic mimicry triggers early recidivation and resistance to adjuvant therapy in esophageal cancer.BMC cancer · 2024Article
- Article
- Theranostic role ofEuropean journal of nuclear medicine and molecular imaging · 2024Article
- BRCA1 mutation promotes sprouting angiogenesis in inflammatory cancer-associated fibroblast of triple-negative breast cancer.Cell death discovery · 2024Article
- Pan-cancer dissection of vasculogenic mimicry characteristic to provide potential therapeutic targets.Frontiers in pharmacology · 2024Article
- Fructose metabolism is unregulated in cancers and placentae.Experimental biology and medicine (Maywood, N.J.) · 2024Review
- Advance in vasculogenic mimicry in ovarian cancer (Review).Oncology letters · 2023Review
- Travelling under pressure - hypoxia and shear stress in the metastatic journey.Clinical & experimental metastasis · 2023Review
8 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Agents that target angiogenesis have shown limited efficacy for human triple-negative breast cancer (TNBC) in clinical trials. Along with endothelium-dependent vessels, there is also vasculogenic mimicry (VM) in the microcirculation of malignant tumors. The role of VM is not completely understood regarding anti-angiogenic treatment. In this study, human TNBC MDA-MB-231 and Hs578T and non-TNBC MCF-7 and BT474 tumor-bearing mice were treated with sunitinib, an anti-angiogenic drug, using a clinically relevant schedule. The drug was administered for one week and then discontinued. Tumor growth and invasion were observed, and the microcirculation patterns were detected with PAS/endomucin staining. Moreover, hypoxia and VM-associated proteins were evaluated with Hypoxyprobe kits and immunohistochemistry, respectively. Sunitinib significantly inhibited tumor growth in the TNBC and non-TNBC tumors. However, MDA-MB-231 and Hs578T tumors regrew and were more aggressive when the treatment was stopped. The discontinuation had no significant effect on the behavior of the non-TNBC MCF-7 and BT474 tumors. The growth of endothelium-dependent vessels in the TNBC MDA-MB-231 and Hs578T tumors were blocked by sunitinib, during which the number of VM channels significantly increased and resulted in a rebound of endothelium-dependent vessels after sunitinib discontinuation. Moreover, the VM-associated proteins VE-cadherin and Twist1 upregulated in the sunitinib-treated MDA-MB-231 and Hs578T tumors. Furthermore, the clinical significance of this upregulation was validated in 174 human breast cancers. The results from human breast cancer specimens indicated that there were more VM-positive TNBC cases than those in non-TNBC cases. HIF-1α, MMP2, VE-cadherin, and Twist1 were also expressed in a higher level in human TNBC compared with non-TNBC. In aconclusion, sunitinib promoted TNBC invasion by VM. The VM status could be helpful to predict the efficacy of anti-angiogenic therapy in patients with TNBC.
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