Article
Cell Biology
Jingyi Cui, Xiaobai Liu, Weiwei Dong, Yunhui Liu, Xuelei Ruan, Mengyang Zhang, Ping Wang, Libo Liu, Yixue Xue
Summary: This study reveals a novel mechanism of the SNORD17/KAT6B/ZNF384 axis in modulating vasculogenic mimicry (VM) development in glioblastoma (GBM), which may provide a new target for the comprehensive treatment of GBM. SNORD17 and ZNF384 were found to promote VM in GBM, while KAT6B inhibited VM in GBM. The interaction between SNORD17 and KAT6B as well as the acetylation of ZNF384 by KAT6B were verified. The binding of ZNF384 to the promoter regions of VEGFR2 and VE-cadherin promoted transcription.
CELL BIOLOGY AND TOXICOLOGY
(2023)
Article
Oncology
Kelsey Maddison, Sam Faulkner, Moira C. Graves, Michael Fay, Nikola A. Bowden, Paul A. Tooney
Summary: This study aimed to quantify the presence of vasculogenic mimicry (VM) in primary and recurrent glioblastoma and determine if these structures express prostate-specific membrane antigen (PSMA). The results showed that only a small proportion of vessels in glioblastoma were VM and they did not express PSMA. The expression of PSMA was also decreased in recurrent tumors compared to primary tumors, as was the total vessel density. VM may contribute to treatment resistance in glioblastoma and further investigation is needed to understand its potential as a treatment target.
Review
Oncology
Kelsey Maddison, Nikola A. Bowden, Moira C. Graves, Paul A. Tooney
Summary: This study aimed to determine the markers consistently attributed to vasculogenic mimicry (VM) and tumour to endothelial transdifferentiation in glioblastoma. It was found that VM lacks expression of CD34 and/or CD31, while tumour to endothelial transdifferentiation expresses CD34 and/or CD31 in addition to other endothelial, stem cell, or tumour cell markers. Further research and characterization of this process are needed.
Article
Biochemistry & Molecular Biology
Cristina Pagano, Giovanna Navarra, Olga Pastorino, Giorgio Avilia, Laura Coppola, Rosa Della Monica, Lorenzo Chiariotti, Tullio Florio, Alessandro Corsaro, Giovanni Torelli, Pasquale Caiazzo, Patrizia Gazzerro, Maurizio Bifulco, Chiara Laezza
Summary: The study demonstrated that N6-isopentenyladenosine (iPA) inhibits the formation of capillary-like structures in glioblastoma cells by modulating the Src/p120-catenin pathway and inhibiting RhoA-GTPase activity, suggesting iPA as a promising novel drug for GBM clinical therapeutics.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Oncology
Huan Wang, Liya Wang, Qiming Zheng, Zeyi Lu, Yuanlei Chen, Danyang Shen, Dingwei Xue, Minxiao Jiang, Lifeng Ding, Jie Zhang, Haiyang Wu, Liqun Xia, Jun Qian, Gonghui Li, Jieyang Lu
Summary: Metabolism reprograming is a hallmark of cancer, and the aberrant metabolism in renal cell carcinoma leads to the accumulation of L-2-hydroxyglurate, which promotes vasculogenic mimicry in renal cancer cells by reducing the expression of PHLDB2 through the activation of the ERK1/2 pathway. These findings suggest a potential therapeutic target for RCC.
INTERNATIONAL JOURNAL OF CANCER
(2021)
Article
Oncology
Paola Franco, Iolanda Camerino, Francesco Merlino, Margherita D'Angelo, Amelia Cimmino, Alfonso Carotenuto, Luca Colucci-D'Amato, Maria Patrizia Stoppelli
Summary: Glioblastoma is a devastating and widespread primary central nervous system tumor that requires innovative and effective therapeutic strategies. This study demonstrates that uPAcyclin, a cyclic decapeptide, can significantly inhibit migration, invasion, and vasculogenic mimicry formation in human glioblastoma cells. These findings suggest that uPAcyclin may be a promising candidate for novel targeted anti-GBM therapies.
Article
Oncology
Min Tao, Xiaoyu Li, Lei He, Xiaoming Rong, Hongxuan Wang, Jingrui Pan, Zijing Lu, Xiaoni Zhang, Ying Peng
Summary: The role of RNA m(6)A modification in glioblastoma (GB) and its impact on the progression of epithelial mesenchymal transition (EMT) and vasculogenic mimicry (VM) have been investigated in this study. The findings suggest that RNA m(6)A methylation suppresses the process of EMT and VM in glioblastoma, providing a new perspective for potential therapeutic targets in GB.
AMERICAN JOURNAL OF CANCER RESEARCH
(2022)
Article
Oncology
Yishan Huang, Chenchen Zhu, Pei Liu, Fan Ouyang, Juanjuan Luo, Chunjiao Lu, Bo Tang, Xiaojun Yang
Summary: Antiangiogenic therapy is a promising clinical strategy for tumor treatment. However, vasculogenic mimicry (VM) formed by invasive tumor cells has been identified as a potential factor for the failure of antiangiogenic therapy. This study demonstrates that L1CAM plays a critical role in VM formation in glioma and may be associated with the resistance of glioma to antiangiogenic therapy.
MOLECULAR ONCOLOGY
(2023)
Review
Medicine, Research & Experimental
Ju Huang, Congcong Wang, Yixuan Hou, Yuanyuan Tian, Yanru Li, Haiying Zhang, Lihong Zhang, Wei Li
Summary: This review discusses the differences between vasculogenic mimicry (VM) and the classical tumor angiogenesis model, as well as the impact of VM on prognosis and survival rates in patients with highly aggressive cancer. The review also highlights the limitations of traditional anti-tumor angiogenesis therapy and the important role of thrombospondin 2 (THBS2) in angiogenesis. Furthermore, the review explores the mechanisms by which THBS2 participates in and regulates tumor VM through the activation of the PI3K/AKT/mTOR signaling pathway.
BIOMEDICINE & PHARMACOTHERAPY
(2023)
Article
Oncology
Shota Shimizu, Ryota Kawahara, Siro Simizu
Summary: This study investigated the role of methionine aminopeptidase-2 (MetAP2) in vasculogenic mimicry (VM) and found that it is critical for VM in human cancer cells. Inhibiting MetAP2 can effectively suppress VM, suggesting its potential as a target for VM inhibition.
Review
Oncology
Xinyu Lin, Sheng Long, Congcong Yan, Xiaofeng Zou, Guoxi Zhang, Junrong Zou, Gengqing Wu
Summary: Angiogenesis is a crucial process in cancer growth and metastasis, but its inhibition can lead to acquired resistance. Vasculogenic mimicry is an alternative mechanism of tumor angiogenesis and is associated with poor prognosis. Inhibiting vasculogenic mimicry may be an effective therapeutic strategy to overcome the limitations of anti-angiogenic treatment when used in combination with other anti-tumor therapies.
FRONTIERS IN ONCOLOGY
(2023)
Article
Immunology
Xiuxiu Liu, Zhenghua Lv, Shengli Zhou, Shifeng Kan, Xianfang Liu, Peihang Jing, Wei Xu
Summary: Macrophage-derived MTDH enhances vascular mimicry formation, cancer cell migration, and invasion through the VEGFA-165/Flt-1 axis, suggesting it could be a potential therapeutic target in HNSCC.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2021)
Article
Cell Biology
Fan Yang, Duo Zhang, Haowen Jiang, Jiangbin Ye, Lin Zhang, Stephen J. Bagley, Jeffery Winkler, Yanqing Gong, Yi Fan
Summary: A compound called toosendanin (TSN) has been found to reprogram macrophages in order to enhance the immune response against glioblastoma (GBM) in mouse models. This compound reverses macrophage-mediated tumor immunosuppression, leading to increased T cell infiltration and activation, and reduced exhaustion.
SCIENCE TRANSLATIONAL MEDICINE
(2023)
Article
Multidisciplinary Sciences
Yuanning Zheng, Francisco Carrillo-Perez, Marija Pizurica, Dieter Henrik Heiland, Olivier Gevaert
Summary: In this study, two deep learning models were used to predict the transcriptional subtypes and prognosis of glioblastoma (GBM) cells from histology images. The results showed consistent associations between spatial cellular organization and patient prognosis. The study also confirmed that transcriptional heterogeneity and cell-state plasticity are key factors in the development of therapeutic resistance in GBM.
NATURE COMMUNICATIONS
(2023)
Article
Biochemistry & Molecular Biology
Francesca Lombardi, Francesca Rosaria Augello, Serena Artone, Mitilda Karoli Gugu, Maria Grazia Cifone, Benedetta Cinque, Paola Palumbo
Summary: TMZ-resistance is a major limitation in the treatment of glioblastoma (GBM). COX-2/PGE2 system plays a role in GBM TMZ resistance, with a dose-dependent up-regulation of COX-2 expression observed in TMZ-treated cells. Combination of NS398 with TMZ can reduce cell proliferation, induce cell cycle arrest and apoptosis, and prevent the up-regulation of COX-2, beta-catenin, MGMT, and SOX-2 in GBM cells.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)