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A Matrigel-Based Tube Formation Assay to Assess the Vasculogenic Activity of Tumor Cells
Published on: September 7, 2011
Therapeutic potential of vasculogenic mimicry in urological tumors
Xinyu Lin1,2, Sheng Long1,2, Congcong Yan1,2
1The First Clinical College, Gannan Medical University, Ganzhou, Jiangxi, China.
Abstract:
Angiogenesis is an essential process in the growth and metastasis of cancer cells, which can be hampered by an anti-angiogenesis mechanism, thereby delaying the progression of tumors. However, the benefit of this treatment modality could be restricted, as most patients tend to develop acquired resistance during treatment. Vasculogenic mimicry (VM) is regarded as a critical alternative mechanism of tumor angiogenesis, where studies have demonstrated that patients with tumors supplemented with VM generally have a shorter survival period and a poorer prognosis. Inhibiting VM may be an effective therapeutic strategy to prevent cancer progression, which could prove helpful in impeding the limitations of lone use of anti-angiogenic therapy when performed concurrently with other anti-tumor therapies. This review summarizes the mechanism of VM signaling pathways in urological tumors, i.e., prostate cancer, clear cell renal cell carcinoma, and bladder cancer. Furthermore, it also summarizes the potential of VM as a therapeutic strategy for urological tumors.
Insights
Vasculogenic mimicry (VM) is a key pathway in tumor growth, offering a target to overcome resistance to anti-angiogenesis therapies. Inhibiting VM may improve outcomes in urological cancers.
Area of Science:
- Oncology
- Cancer Biology
- Urology
Background:
- Angiogenesis is crucial for tumor growth and metastasis.
- Anti-angiogenesis therapies face limitations due to acquired resistance.
- Vasculogenic mimicry (VM) is an alternative tumor angiogenesis pathway linked to poorer prognosis.
Purpose of the Study:
- To review VM signaling pathways in urological tumors.
- To explore VM as a therapeutic strategy for prostate, kidney, and bladder cancers.
- To address limitations of anti-angiogenic therapy by considering VM inhibition.
Main Methods:
- Literature review of VM mechanisms in urological cancers.
- Analysis of VM signaling pathways.
- Evaluation of VM as a therapeutic target.
Main Results:
- VM is a significant alternative angiogenesis mechanism in tumors.
- VM presence correlates with shorter survival and poorer prognosis in urological cancers.
- Targeting VM may enhance anti-tumor therapy efficacy.
Conclusions:
- VM is a critical factor in urological tumor progression.
- Inhibiting VM presents a promising therapeutic strategy.
- Combining VM inhibition with anti-angiogenic therapy could overcome treatment resistance.
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