ArticleInternational journal of women's health2023
Molecular Mechanisms Behind Vascular Mimicry as the Target for Improved Breast Cancer Management.
Article in International journal of women's health, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Vasculogenic mimicry and breast cancer prognosis: Insights into predictive model development.Oncology letters · 2026Article
- Multi-omic analysis of the liver-breast axis reveals key hepatic mediators of breast cancer progression.Science China. Life sciences · 2026Review
- Article
- The FOXC2-LAMA4 Axis Orchestrates Vasculogenic Mimicry and Immunosuppressive Niche Formation to Drive Metastatic Cascade in Renal Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single nucleotide polymorphism-based analysis of linkage disequilibrium and runs of homozygosity patterns of indigenous sheep in the southern Taklamakan desert.BMC genomics · 2025Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Breast cancer has a high incidence and mortality rate in women due to metastasis and drug resistance which is associated with vasculogenic mimicry (VM). We purposed to explore VM formulation in breast cancer and mechanism of which is involved in EphA2/PIK3R1/CTNNB1 in the present study. Methods: The expression of EphA2/PIK3R1/CTNNB1 and breast cancer patient prognosis was analyzed from TCGA data, both gene and protein expression as well as VM were measured in human breast cancer tissue samples collected in our study. The relationship between EphA2/PIK3R1/CTNNB1 and the formation of VM in breast cancer and its possible regulatory mechanism was explored. Results: The results of the bioinformatics analysis based on TCGA showed that the expression of PIK3R1/ CTNNB1/ PECAM1 (CD31) in tumor tissues was significantly lower than that in normal tissues. EphA2 was positively correlated with PIK3R1, PIK3R1 with CTNNB1, and CTNNB1 with PECAM1 expression in breast cancer tissues. The results of detection in breast cancer and adjacent tissues indicated that the expression of EphA2/PIK3R1/CTNNB1 in cancer tissues was significantly lower than that in adjacent tissues. The expression of PIK3R1 was positively correlated with EphA2 and CTNNB1 expression, respectively, as well as EphA2 expression correlated with CTNNB1 expression positively. VM formation was significantly increased in breast cancer tissues compared with adjacent tissues. Conclusion: Our results suggested that the formation of VM in breast cancer may be related to the EphA2/PIK3R1/CTNNB1 molecular signaling pathway.
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