Dual VEGF/PDGF knockdown suppresses vasculogenic mimicry formation in choroidal melanoma cells via the Wnt5a/β-catenin/AKT signaling pathway

Yuan, Yingying; Geng, Bochao; Xu, Xiaoyan; Zhao, Han; Bai, Jian; Dou, Zhizhi; Jia, Shaoyou; Yu, Xiaoling; Luo, Wenjuan

doi:10.1016/j.acthis.2021.151842

Cited by 5 publications

(2 citation statements)

References 46 publications

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“…It is notable that EMT, angiogenesis, hypoxia and NOTCH signaling were positively correlated with VM in all tumors ( Figure 2C ). WNT/β-catenin and NOTCH signaling pathways were confirmed to be involved in the process of EMT and VM in ( Benjakul et al, 2022 ; Yuan et al, 2022 ). Cancer hallmarks such as P53 signaling, glycolysis, KRAS signaling pathways, and immune-related pathways such as TNF-α, TGF-β, IL2/STAT5, IL-6/JAK/STAT3, interferon-γ response, and inflammatory response pathways were also positively associated with VM ( Figures 2B,C ).…”

Section: Resultsmentioning

confidence: 86%

Pan-cancer dissection of vasculogenic mimicry characteristic to provide potential therapeutic targets

Tang,

Chen,

Liu

et al. 2024

Front. Pharmacol.

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Introduction:Vasculogenic mimicry (VM) represents a novel form of tumor angiogenesis that is associated with tumor invasiveness and drug resistance. However, the VM landscape across cancer types remains poorly understood. In this study, we elucidate the characterizations of VM across cancers based on multi-omics data and provide potential targeted therapeutic strategies.Methods:Multi-omics data from The Cancer Genome Atlas was used to conduct comprehensive analyses of the characteristics of VM related genes (VRGs) across cancer types. Pan-cancer vasculogenic mimicry score was established to provide a depiction of the VM landscape across cancer types. The correlation between VM and cancer phenotypes was conducted to explore potential regulatory mechanisms of VM. We further systematically examined the relationship between VM and both tumor immunity and tumor microenvironment (TME). In addition, cell communication analysis based on single-cell transcriptome data was used to investigate the interactions between VM cells and TME. Finally, transcriptional and drug response data from the Genomics of Drug Sensitivity in Cancer database were utilized to identify potential therapeutic targets and drugs. The impact of VM on immunotherapy was also further clarified.Results:Our study revealed that VRGs were dysregulated in tumor and regulated by multiple mechanisms. Then, VM level was found to be heterogeneous among different tumors and correlated with tumor invasiveness, metastatic potential, malignancy, and prognosis. VM was found to be strongly associated with epithelial-mesenchymal transition (EMT). Further analyses revealed cancer-associated fibroblasts can promote EMT and VM formation. Furthermore, the immune-suppressive state is associated with a microenvironment characterized by high levels of VM. VM score can be used as an indicator to predict the effect of immunotherapy. Finally, seven potential drugs targeting VM were identified.Conclusion:In conclusion, we elucidate the characteristics and key regulatory mechanisms of VM across various cancer types, underscoring the pivotal role of CAFs in VM. VM was further found to be associated with the immunosuppressive TME. We also provide clues for the research of drugs targeting VM. Our study provides an initial overview and reference point for future research on VM, opening up new avenues for therapeutic intervention.

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Section: Resultsmentioning

confidence: 86%

Pan-cancer dissection of vasculogenic mimicry characteristic to provide potential therapeutic targets

Tang,

Chen,

Liu

et al. 2024

Front. Pharmacol.

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“…A recent study investigated how VEGF/PDGF pathway controls vascular mimicry in a Wnt5/β catenin manner. Dual knockdown of VEGF/PDGF inhibited vascular mimicry and resulted in cell apoptosis [ 79 ]. As discussed here, there remains controversy in the gene expression and specific markers for distinguishing the endothelial and melanoma cells that contribute to vasculogenic mimicry.…”

Section: How Do Tumour Blood Vessels Form In Melanoma?mentioning

confidence: 99%

Melanoma Tumour Vascularization and Tissue-Resident Endothelial Progenitor Cells

Hashemi

Dight

Khosrotehrani

et al. 2022

Cancers

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The aggressiveness of solid cancers, such as melanoma, relies on their metastatic potential. It has become evident that this key cause of mortality is largely conferred by the tumour-associated stromal cells, especially endothelial cells. In addition to their essential role in the formation of the tumour vasculature, endothelial cells significantly contribute to the establishment of the tumour microenvironment, thus enabling the dissemination of cancer cells. Melanoma tumour vascularization occurs through diverse biological processes. Vasculogenesis is the formation of de novo blood vessels from endothelial progenitor cells (EPCs), and recent research has shown the role of EPCs in melanoma tumour vascularization. A more detailed understanding of the complex role of EPCs and how they contribute to the abnormal vessel structures in tumours is of importance. Moreover, anti-angiogenic drugs have a limited effect on melanoma tumour vascularization, and the role of these drugs on EPCs remains to be clarified. Overall, targeting cancer vasculature remains a challenge, and the role of anti-angiogenic drugs and combination therapies in melanoma, a focus of this review, is an area of extensive exploration.

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Artesunate inhibits vasculogenic mimicry in choroidal melanoma through HIF-1 α/ VEGF/PDGF pathway

Ma,

Xu,

Zhu

et al. 2024

Acta Histochemica

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Dual VEGF/PDGF knockdown suppresses vasculogenic mimicry formation in choroidal melanoma cells via the Wnt5a/β-catenin/AKT signaling pathway

Cited by 5 publications

References 46 publications

Pan-cancer dissection of vasculogenic mimicry characteristic to provide potential therapeutic targets

Pan-cancer dissection of vasculogenic mimicry characteristic to provide potential therapeutic targets

Melanoma Tumour Vascularization and Tissue-Resident Endothelial Progenitor Cells

Artesunate inhibits vasculogenic mimicry in choroidal melanoma through HIF-1 α/ VEGF/PDGF pathway

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