Association of aquaporin‑1 with tumor migration, invasion and vasculogenic mimicry in glioblastoma multiforme

Yang, Wanyong; Tan, Zefeng; Dong, Dawei; Ding, Yan; Meng, Heng; Zhao, Ying; Xin, Xiufeng; Bi, Wei

doi:10.3892/mmr.2017.8265

Cited by 12 publications

(15 citation statements)

References 25 publications

(25 reference statements)

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“…In lung cancer cells, AQP1 knockdown had inhibitory effects on cancer cell proliferation and migration along with the downregulation of MMP‐9 expression 28 . It was also demonstrated that silencing of AQP1 expression resulted in decreased MMP‐9 expression in GBM cells 29 . In this study, forced expression of AQP1 also significantly upregulated MMP‐9 activities (Figure 3M).…”

Section: Discussionsupporting

confidence: 60%

Aquaporin 1 elicits cell motility and coordinates vascular bed formation by downregulating thrombospondin type‐1 domain‐containing 7A in glioblastoma

et al. 2020

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Background Aquaporin (AQP) 1 expression has been linked with tumor malignancy but its role in glioblastoma (GBM), a lethal glioma, remains to be clarified. Methods AQP1 expression was examined in 33 human GBM specimens by immunohistochemistry. GBM cells (U251 and U87) that stably express AQP1 were established and used for cellular proliferation, migration, invasion, and vascular tube formation assays. The GeneChip assay was used to identify differentially expressed genes in AQP1‐expressing cells. Results AQP1 was expressed only in tumor cells. AQP1 dose‐dependently accelerated cell migration and invasion, but not proliferation, in GBM cell lines. AQP1 also upregulated cathepsin B, focal adhesion kinase and activities of matrix metalloproteinase 9. AQP1 in GBM cells induced wall thickness of ECV304, vascular endothelial cells, in a contact‐dependent manner. Downregulation of thrombospondin type 1 domain containing 7A (THSD7A) was identified in AQP1‐expressing GBM cells in vitro, and was negatively correlated with AQP1 expression in human GBM specimens. Conclusion AQP1 is involved in tumor malignancy by facilitating the migration and invasion of GBM cells, and promoting the formation of vascular beds that are characteristic of GBM by downregulating THSD7A.

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Section: Discussionsupporting

confidence: 60%

Aquaporin 1 elicits cell motility and coordinates vascular bed formation by downregulating thrombospondin type‐1 domain‐containing 7A in glioblastoma

et al. 2020

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“…83 Aquaporin-1 may play a role in VM in glioblastoma, and it can be used as a new diagnostic biomarker and a potential therapeutic target. 84 In oligodendroglioma, downregulation of galectin-1 gene expression, a significant decrease in brain expressed X-linked 2 expression, and inhibition of VM may present new therapeutic strategies for reducing chemotherapy resistance. 85 A histone deacetylase inhibitor has also been identified as a promising candidate for VM inhibition in glioblastoma.…”

Section: Cytokine Familymentioning

confidence: 99%

<p>Advances and Prospects of Vasculogenic Mimicry in Glioma: A Potential New Therapeutic Target?</p>

Cai

Liu

et al. 2020

OTT

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Vasculogenic mimicry (VM) is the formation of a "vessel-like" structure without endothelial cells. VM exists in vascular-dependent solid tumors and is a special blood supply source involved in the highly invasive tumor progression. VM is observed in a variety of human malignant tumors and is closely related to tumor proliferation, invasion, and recurrence. Here, we review the mechanism, related signaling pathways, and molecular regulation of VM in glioma and discuss current research problems and the potential future applications of VM in glioma treatment. This review may provide a new viewpoint for glioma therapy.

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“…Recent studies, have highlighted the important role of ion channels in GBM cell proliferation and aggressiveness (Sforna et al, 2017; Wong et al, 2018; Yang et al, 2017, 2018; D’Alessandro et al, 2018). In particular, it has been shown that the swelling-activated Cl − current is over-expressed in GBM cell lines (Catacuzzeno et al, 2014; Sforna et al, 2017), and contributes substantially to cell proliferation through activation of JAK2/STAT3 and PI3K/AKT signaling pathways (Wong et al, 2018).…”

Section: Gbm-induced Abnormal Cell-proliferationmentioning

confidence: 99%

Dexamethasone in Glioblastoma Multiforme Therapy: Mechanisms and Controversies

Cenciarini

Valentino

Belia

et al. 2019

Front. Mol. Neurosci.

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Glioblastoma multiforme (GBM) is the most common and malignant of the glial tumors. The world-wide estimates of new cases and deaths annually are remarkable, making GBM a crucial public health issue. Despite the combination of radical surgery, radio and chemotherapy prognosis is extremely poor (median survival is approximately 1 year). Thus, current therapeutic interventions are highly unsatisfactory. For many years, GBM-induced brain oedema and inflammation have been widely treated with dexamethasone (DEX), a synthetic glucocorticoid (GC). A number of studies have reported that DEX also inhibits GBM cell proliferation and migration. Nevertheless, recent controversial results provided by different laboratories have challenged the widely accepted dogma concerning DEX therapy for GBM. Here, we have reviewed the main clinical features and genetic and epigenetic abnormalities underlying GBM. Finally, we analyzed current notions and concerns related to DEX effects on cerebral oedema, cancer cell proliferation and migration and clinical outcome.

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Association of aquaporin‑1 with tumor migration, invasion and vasculogenic mimicry in glioblastoma multiforme

Cited by 12 publications

References 25 publications

Aquaporin 1 elicits cell motility and coordinates vascular bed formation by downregulating thrombospondin type‐1 domain‐containing 7A in glioblastoma

Aquaporin 1 elicits cell motility and coordinates vascular bed formation by downregulating thrombospondin type‐1 domain‐containing 7A in glioblastoma

<p>Advances and Prospects of Vasculogenic Mimicry in Glioma: A Potential New Therapeutic Target?</p>

Dexamethasone in Glioblastoma Multiforme Therapy: Mechanisms and Controversies

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