Short-term anti-vascular endothelial growth factor treatment elicits vasculogenic mimicry formation of tumors to accelerate metastasis

Xu, Yuan; Qin, Li; Li, Xiaoyu; Yang, Qin; Xu, Wei; Gao-lin, Liu

doi:10.1186/1756-9966-31-16

Cited by 142 publications

(126 citation statements)

References 27 publications

(20 reference statements)

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“…Several mechanisms have been proposed to explain this, many of which offer potential clues about therapeutic strategies to reverse this effect (42). These include induced pericyte and PDGF activation (43)(44)(45)(46), c-met pathway promotion (47)(48)(49)(50), control of vascular mimicry (51,52), hypoxia and HIF1a activation (53), altered metabolic function (54), collagen signaling (55), increases in IL12b (56), IL8 (57), HTATIP2 (58,59), heparinases (60), and Semaphorins 3A and 3E (refs. 61, 62; for review, see ref.…”

Section: Tim and The Tme: Lessons From Angiogenesis Inhibitorsmentioning

confidence: 99%

Prodding the Beast: Assessing the Impact of Treatment-Induced Metastasis

Ebos

2015

Cancer Research

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The arsenal of treatments for most cancers fit broadly into the categories of surgery, chemotherapy, radiation, and targeted therapy. All represent proven and successful strategies, yet each can trigger local (tumor) and systemic (host) processes that elicit unwanted, often opposing, influences on cancer growth. Under certain conditions, nearly all cancer treatments can facilitate metastatic spread, often in parallel (and sometimes in clear contrast) with tumor reducing benefits. The paradox of treatment-induced metastasis (TIM) is not new. Supporting preclinical studies span decades, but are often overlooked. With recent evidence of prometastatic effects following treatment with tar-

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Section: Tim and The Tme: Lessons From Angiogenesis Inhibitorsmentioning

confidence: 99%

Prodding the Beast: Assessing the Impact of Treatment-Induced Metastasis

Ebos

2015

Cancer Research

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“…The number of red blood cells in the tubular structure is ≥1. All the steps were performed as previously described (22).…”

Section: Clinical Tissue Samples and Immunohistochemistry (Ihc)mentioning

confidence: 99%

Vasculogenic mimicry in bladder cancer and its association with the aberrant expression of ZEB1

Mao

Wang

et al. 2018

Oncol Lett

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Abstract. The aim of the present study was to investigate the associations between vasculogenic mimicry (VM) and zinc finger E-box binding homeobox 1 (ZEB1) in bladder cancer. VM structure and ZEB1 expression were analyzed by cluster of differentiation 34/periodic acid Schiff (PAS) double staining and immunohistochemical staining in 135 specimens from patients with bladder cancer, and a further 12 specimens from normal bladder tissues. Three-dimensional (3-D) culture was used to detect VM formation in the bladder transitional cancer cell lines UM-UC-3 and J82, and the immortalized human bladder epithelium cell line SV-HUC-1 in vitro. ZEB1 expression in these cell lines was compared by reverse transcription-quantitative polymerase chain reaction and western blot assays. In addition, small interfering RNA was used to inhibit ZEB1 in UM-UC-3 and J82 cells, followed by 3-D culturing of treated cell lines. As a result, VM was observed in 31.1% of specimens from bladder cancer tissues, and cases with high ZEB1 expression accounted for 60.0% of patients with bladder cancer. In addition, ZEB1 expression was closely associated with VM (r=0.189; P<0.05), and also increased as the grade and stage of the tumor developed. In an in vitro assay, UM-UC-3 and J82 cells exhibited VM formation, however, SV-HUC-1 did not. Furthermore, VM-forming cancer cell lines UM-UC-3 and J82 exhibited higher ZEB1 expression. Notably, VM formation was inhibited following knockdown of ZEB1. In conclusion, ZEB1 may be associated with VM in bladder cancer and serve an important role in the process of VM formation. However, its detailed mechanism requires further study.

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“…The antiangiogenic drug bevacizumab (Avastin) has become one of the most popular vascular-targeted therapeutic drugs for several types of tumors, including gliomas (2). However, this traditional antiangiogenic drug also accelerates metastasis, together with marked hypoxia and an alternative blood supply -vasculogenic mimicry (VM) (3). VM consists of laminin-rich networks that can be stained with periodic acid-Schiff (PAS) in vivo and forms extracellular matrix (ECM)-rich tubular networks on Matrigel that mimic conventional angiogenesis in vitro.…”

Section: Introductionmentioning

confidence: 99%

Mammalian target of rapamycin signaling is involved in the vasculogenic mimicry of glioma via hypoxia-inducible factor-1α

Min

Sun

et al. 2014

Oncology Reports

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Abstract. The mammalian target of rapamycin (mTOR) is a crucial regulator in malignant gliomas. Vasculogenic mimicry (VM) describes functional channels established by highly malignant tumor cells that is different from endothelium-lined blood vessels. Our previous studies confirmed the existence and clinical significance of VM in medulloblastoma and glioblastoma. In the present study, by immunohistochemical and CD34/PAS histochemical double-staining, 34 cases (26.8%) with VM structures were identified among a total of 127 glioma cases, and these VM structures were associated with mTOR expression in the glioma specimens. In vitro, U87 malignant glioblastoma cells formed tube structures similar to HUVECs on Matrigel in 3D culture, and mTOR-specific inhibitor rapamycin inhibited VM formation in the U87 malignant glioblastoma cells under both normoxia and hypoxia. In addition, rapamycin and mTOR siRNA inhibited molecules in the signaling cascade of VM formation, particularly HIF-1α. Taken together, our results demonstrated that mTOR signaling is involved in VM formation, and may be a potential therapeutic target for gliomas.

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Short-term anti-vascular endothelial growth factor treatment elicits vasculogenic mimicry formation of tumors to accelerate metastasis

Cited by 142 publications

References 27 publications

Prodding the Beast: Assessing the Impact of Treatment-Induced Metastasis

Prodding the Beast: Assessing the Impact of Treatment-Induced Metastasis

Vasculogenic mimicry in bladder cancer and its association with the aberrant expression of ZEB1

Mammalian target of rapamycin signaling is involved in the vasculogenic mimicry of glioma via hypoxia-inducible factor-1α

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