Caveolin-1 promotes tumor cell proliferation and vasculogenic mimicry formation in human glioma

Chen, Wenli; Cheng, Xing; Wang, Xiaobo; Hu, Wenjie; Wang, Jinshan; Liao, Chengde

doi:10.1590/1414-431x2020e10653

Cited by 4 publications

(2 citation statements)

References 33 publications

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“…Notably, expression of CAV1 was significantly upregulated in high-grade glioma patients, and high expression of CAV1 is associated with a poor prognosis in glioma. Previous studies have demonstrated that CAV1 promotes glioma cell proliferation and vasculogenic mimicry and regulates focal adhesion by effecting FAK phosphorylation [ 26 , 39 ]. Therefore, our study indicated that LINC01003 is a positive regulator in the CAV1/FAK signaling pathway in glioma cells.…”

Section: Discussionmentioning

confidence: 99%

m6A-mediated upregulation of LINC01003 regulates cell migration by targeting the CAV1/FAK signaling pathway in glioma

Zhu

Yang

et al. 2023

Biol Direct

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Background Long non-coding RNAs (lncRNAs) play important roles in the progression of glioma. Here, we examined the potential functions of a lncRNA, LINC01003, in glioma and characterized the underlying molecular mechanisms. Methods The GEIPA2 and Chinese Glioma Genome Atlas (CCGA) databases were employed to analyze gene expression and the overall survival curve in patients with glioma. The functions of LINC01003 in glioma growth and migration were assessed by loss-of-function experiments in vitro and in vivo. RNA sequencing was used to determine the signaling pathways effected by LINC01003. Bioinformatics analysis and RNA immunoprecipitation (RIP) assays were used to explore the mechanism underlying the N6-methyladenine (m6A) modification-dependent upregulation of LINC01003 in glioma. Results LINC01003 expression was upregulated in glioma cell lines and tissues. Higher LINC01003 expression predicted shorter overall survival time in glioma patients. Functionally, LINC01003 knockdown inhibited the cell cycle and cell proliferation and migration in glioma cells. Mechanistically, RNA sequencing revealed that LINC01003 mediated the focal adhesion signaling pathway. Furthermore, LINC01003 upregulation is induced by m6A modification regulated by METTL3. Conclusion This study characterized LINC01003 as a lncRNA that contributes to tumorigenesis in glioma and demonstrated that the LINC01003-CAV1-FAK axis serves as a potential therapeutic target for glioma.

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Section: Discussionmentioning

confidence: 99%

m6A-mediated upregulation of LINC01003 regulates cell migration by targeting the CAV1/FAK signaling pathway in glioma

Zhu

Yang

et al. 2023

Biol Direct

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“…VM mimics the function of blood vessels and transports plasma and blood cells, providing an alternative mechanism to supply malignant tumors with adequate blood. The pathological grade of glioma increases with the number of VM [ 4 ]. The presence of VM greatly hinders the treatment of GBM with anti-angiogenic drugs [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

The mechanism of BUD13 m6A methylation mediated MBNL1-phosphorylation by CDK12 regulating the vasculogenic mimicry in glioblastoma cells

et al. 2022

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Vasculogenic mimicry (VM) is an endothelium-independent tumor microcirculation that provides adequate blood supply for tumor growth. The presence of VM greatly hinders the treatment of glioblastoma (GBM) with anti-angiogenic drugs. Therefore, targeting VM formation may be a feasible therapeutic strategy for GBM. The research aimed to evaluate the roles of BUD13, CDK12, MBNL1 in regulating VM formation of GBM. BUD13 and CDK12 were upregulated and MBNL1 was downregulated in GBM tissues and cells. Knockdown of BUD13, CDK12, or overexpression of MBNL1 inhibited GBM VM formation. METTL3 enhanced the stability of BUD13 mRNA and upregulated its expression through m6A methylation. BUD13 enhanced the stability of CDK12 mRNA and upregulated its expression. CDK12 phosphorylated MBNL1, thereby regulating VM formation of GBM. The simultaneous knockdown of BUD13, CDK12, and overexpression of MBNL1 reduced the volume of subcutaneously transplanted tumors in nude mice and prolonged the survival period. Thus, the BUD13/CDK12/MBNL1 axis plays a crucial role in regulating VM formation of GBM and provides a potential target for GBM therapy.

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Assessment of Serum Hypoxia Biomarkers Pre- and Post-radiotherapy in Patients with Brain Tumors

et al. 2022

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Hypoxia is a prevalent hallmark of many malignant neoplasms. The aim was to assess the serum hypoxia biomarkers HIF-1α, VEGF, osteopontin, erythropoietin, caveolin-1, GLUT-1, and LDH pre- and post-radiotherapy in patients with brain tumors. The study was conducted on 120 subjects were divided into two groups: group I: 40 healthy volunteers as control group. Group II: 80 brain tumor patients were subdivided into glioblastoma subgroup: 40 glioblastoma patients, meningioma subgroup: 40 malignant meningioma patients. Two venous blood samples were collected from every patient prior to and following RT and one sample from controls. Biomarkers were assayed by ELISA. In glioblastoma subgroup, HIF-1α, VEGF, and LDH were significantly increased after RT. On the contrary, these biomarkers were significantly decreased after RT in malignant meningioma subgroup. Osteopontin was significantly increased after RT in both subgroups. Regarding erythropoietin, it was significantly decreased in both subgroups when compared to before RT. Caveolin-1 showed a significant increase in glioblastoma subgroup after RT comparing to before RT. GLUT-1 was significantly increased after RT in both subgroups comparing to before RT. Association of significant elevation of hypoxia biomarkers either pre- or post-RT with aggressive tumor such as glioblastoma indicates that, they are markers of malignancy and may have a role in tumor development and progression.

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Caveolin-1 promotes tumor cell proliferation and vasculogenic mimicry formation in human glioma

Cited by 4 publications

References 33 publications

m6A-mediated upregulation of LINC01003 regulates cell migration by targeting the CAV1/FAK signaling pathway in glioma

m6A-mediated upregulation of LINC01003 regulates cell migration by targeting the CAV1/FAK signaling pathway in glioma

The mechanism of BUD13 m6A methylation mediated MBNL1-phosphorylation by CDK12 regulating the vasculogenic mimicry in glioblastoma cells

Assessment of Serum Hypoxia Biomarkers Pre- and Post-radiotherapy in Patients with Brain Tumors

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