Vasculogenic mimicry: a novel target for glioma therapy

Chen, Yin Sheng; Chen, Zhong Ping

doi:10.5732/cjc.012.10292

Cited by 73 publications

(62 citation statements)

References 49 publications

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“…This finding might show that VM was more prevalent in ACC with higher malignancy, which was similar to that in other tumors . Actually, VM has been reported to be a signature of poor prognosis in malignant tumors, such as ovarian cancer, glioma, renal cell carcinoma and hepatocellular carcinoma . In the present retrospective study of 46 patients with ACC, our findings were also consistent with the aforementioned studies.…”

Section: Discussionsupporting

confidence: 92%

Vasculogenic mimicry plays an important role in adrenocortical carcinoma

et al. 2016

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Abbreviations & Acronyms ACC = adrenocortical carcinoma CCK-8 = Cell Counting Kit-8 OS = overall survival PAS = periodic acid-Schiff PBS = phosphate-buffered saline qPCR = quantitative polymerase chain reaction siRNA = small interfering ribonucleic acid TKI = tyrosine kinase inhibitor VEGF = vascular endothelial growth factor VEGFR-2 = vascular endothelial growth factor receptor 2 VM = vasculogenic mimicry Objectives: To determine the prognostic role of vasculogenic mimicry in adrenocortical carcinoma, and to explore its relationship with vascular endothelial growth factor receptor 2 expression. Methods: A total of 46 samples of adrenocortical carcinoma were collected and reviewed. Vasculogenic mimicry and vascular endothelial growth factor receptor 2 were detected by immunohistochemistry and double staining. Survival analysis was carried out to access pronostic significance. Three-dimensional culture method was applied to test the ability of vasculogenic mimicry formation by adrenocortical carcinoma cell lines SW-13 and H295R. Quantitative polymerase chain reaction and western blotting were used to monitor the expression of vascular endothelial growth factor receptor 2 in SW-13 and H295R. After being treated with specific inhibitor or small interfering ribonucleic acid to downregulate expression of vascular endothelial growth factor receptor 2, vasculogenic mimicry formation and cell prolifration of SW-13 cells were evaluated by 3-D culture and Cell Counting Kit-8 methods. Results: Vasculogenic mimicry was observed in 19 of the 46 (41.30%) adrenocortical carcinoma samples. Both vasculogenic mimicry and vascular endothelial growth factor receptor 2 expressions showed a positive association with Weiss score and TNM stage, whereas vascular endothelial growth factor receptor 2 was also associated with tumor size (all P < 0.05). Vasculogenic mimicry was closely correlated with vascular endothelial growth factor receptor 2 expressions (r = 0.470, P < 0.01). The median overall survival of patients with vasculogenicmimicry-positive or vascular endothelial growth factor receptor 2-positive was shorter than that of patients with vasculogenic mimicry-negative or vascular endothelial growth factor receptor 2-negative (P = 0.001 and 0.028, respectively). The vasculogenic mimicry-forming SW-13 cells expressed higher levels of vascular endothelial growth factor receptor 2 than that of H295R, which was unable to form vasculogenic mimicry on Matrigel. However, downregulation of vascular endothelial growth factor receptor 2 only decreased cell proliferation, but not vasculogenic mimicry formation by SW-13 cells. Conclusions: Vasculogenic mimicry and overexpression of vascular endothelial growth factor receptor 2 seem to correlate with poor prognostic outcomes in adrenocortical carcinoma. Anti-angiogenesis treatments targeting vascular endothelial growth factor receptor 2 should be combined with therapies targeting vasculogenic mimicry in adrenocortical carcinoma.

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Section: Discussionsupporting

confidence: 92%

Vasculogenic mimicry plays an important role in adrenocortical carcinoma

et al. 2016

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“…Tumor blood vessel formation is caused not only by angiogenesis dependent on host endothelial cells but also by VM, which plays an equally substantial role in this process161718. VM, which refers to a process whereby tumor cells directly line up to form blood vessels, was first reported in melanoma by Hendrix and colleagues in 19994.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia-induced vasculogenic mimicry formation in human colorectal cancer cells: Involvement of HIF-1a, Claudin-4, and E-cadherin and Vimentin

Zong

Shi

et al. 2016

Sci Rep

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Vasculogenic mimicry (VM) plays an important role in colorectal cancer (CRC) metastasis, and both hypoxia and the epithelial-mesenchymal transition (EMT) are necessary for VM. In this study, HIF-1α expression was upregulated in the VM-positive CRC cell line HCT-116 and thereby affected the expression of the EMT-related markers Claudin-4, E-cadherin (E-cd) and Vimentin(VIM). SB431542 and U0126EtOH, which can inhibit of EMT were used to treat HCT-116 and HCT-8 in these experiments. Both of the inhibitors had significant effect on EMT markers and the formations of VM in CRC cells. In addition, knockdown of HIF-1α in the HCT-116 cells inhibited their capacity for VM. Our study reveals a regulatory role for HIF-1α in VM and suggests that targeting either HIF-1α or EMT may be a valuable strategy for the elimination of CRC metastasis.

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“…The presence of VM in glioblastoma has been confirmed by many reports [7–10]. Like the anti-angiogenic strategy, anti-vascular mimicry is considered as a novel targeting strategy for the treatment of glioma [9]. …”

Section: Introductionmentioning

confidence: 89%

Multi-targeting NGR-modified liposomes recognizing glioma tumor cells and vasculogenic mimicry for improving anti-glioma therapy

et al. 2016

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Like the anti-angiogenic strategy, anti-vascular mimicry is considered as a novel targeting strategy for glioma. In the present study, we used NGR as a targeting ligand and prepared NGR-modified liposomes containing combretastatin A4 (NGR-SSL-CA4) in order to evaluate their potential targeting of glioma tumor cells and vasculogenic mimicry (VM) formed by glioma cells as well as their anti-VM activity in mice with glioma tumor cells. NGR-SSL-CA4 was prepared by a thin-film hydration method. The in vitro targeting of U87-MG (human glioma tumor cells) by NGR-modified liposomes was evaluated. The in vivo targeting activity of NGR-modified liposomes was tested in U87-MG orthotopic tumor-bearing nude mice. The anti-VM activity of NGR-SSL-CA4 was also investigated in vitro and in vivo. The targeting activity of the NGR-modified liposomes was demonstrated by in vitro flow cytometry and in vivo biodistribution. The in vitro anti-VM activity of NGR-SSL-CA4 was indicated in a series of cell migration and VM channel experiments. NGR-SSL-CA4 produced very marked anti-tumor and anti-VM activity in U87-MG orthotopic tumor-bearing mice in vivo. Overall, the NGR-SSL-CA4 has great potential in the multi-targeting therapy of glioma involving U87-MG cells, and the VM formed by U87-MG cells as well as endothelial cells producing anti-U87-MG cells, and anti-VM formed by U87-MG cells as well as anti-endothelial cell activity.

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Vasculogenic mimicry: a novel target for glioma therapy

Cited by 73 publications

References 49 publications

Vasculogenic mimicry plays an important role in adrenocortical carcinoma

Vasculogenic mimicry plays an important role in adrenocortical carcinoma

Hypoxia-induced vasculogenic mimicry formation in human colorectal cancer cells: Involvement of HIF-1a, Claudin-4, and E-cadherin and Vimentin

Multi-targeting NGR-modified liposomes recognizing glioma tumor cells and vasculogenic mimicry for improving anti-glioma therapy

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