C-type natriuretic peptide-modified lipid vesicles: fabrication and use for the treatment of brain glioma

Wu, Jia-Shuan; Mu, Li-Min; Bu, Ying-Zi; Liu, Lei; Yan, Yan; Hu, Yingjie; Bai, Jing; Zhang, Jingying; Lu, Weiyue; Lü, Wan-Liang

doi:10.18632/oncotarget.16641

Cited by 5 publications

(3 citation statements)

References 51 publications

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“…Concerning possible actions of CNP in glial tissues, there is a strong body of evidence 235:1 that cGMP, a downstream mediator of CNP activity and more responsive to CNP than either ANP or BNP (Deschepper & Picard 1994), regulates several crucial intercellular actions including Na + /H + exchangers, neurotransmitter re-uptake, gap junctions, cell pH and brain cell water content (Kim et al 2010). In this context, it is important to note that dexamethasone mitigates cerebral glioma tumour oedema, a cell type highly responsive to CNP (Eguchi et al 1992, Wu et al 2017. Conceivably, this well-described pharmacological action of dexamethasone is mediated at least in part by CNP which could have therapeutic implications now that CNP agonists are available for use in humans.…”

Section: Discussionmentioning

confidence: 99%

Dexamethasone increases production of C-type natriuretic peptide in the sheep brain

Wilson

McNeill

Barrell

et al. 2017

Journal of Endocrinology

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Although C-type natriuretic peptide (CNP) has high abundance in brain tissues and cerebrospinal fluid (CSF), the source and possible factors regulating its secretion within the central nervous system (CNS) are unknown. Here we report the dynamic effects of a single IV bolus of dexamethasone or saline solution on plasma, CSF, CNS and pituitary tissue content of CNP products in adult sheep, along with changes in CNP gene expression in selected tissues. Both CNP and NTproCNP (the amino-terminal product of proCNP) in plasma and CSF showed dose-responsive increases lasting 12-16 h after dexamethasone, whereas other natriuretic peptides were unaffected. CNS tissue concentrations of CNP and NTproCNP were increased by dexamethasone in all of the 12 regions examined. Abundance was highest in limbic tissues, pons and medulla oblongata. Relative to controls, CNP gene expression () was upregulated by dexamethasone in 5 of 7 brain tissues examined. Patterns of responses differed in pituitary tissue. Whereas the abundance of CNP in both lobes of the pituitary gland greatly exceeded that of brain tissues, neither CNP nor NTproCNP concentration was affected by dexamethasone, despite an increase in expression. This is the first report of enhanced production and secretion of CNP in brain tissues in response to a corticosteroid. Activation of CNP secretion within CNS tissues by dexamethasone, not exhibited by other natriuretic peptides, suggests an important role for CNP in settings of acute stress. Differential findings in pituitary tissues likely relate to altered processing of proCNP storage and secretion.

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Section: Discussionmentioning

confidence: 99%

Dexamethasone increases production of C-type natriuretic peptide in the sheep brain

Wilson

McNeill

Barrell

et al. 2017

Journal of Endocrinology

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“…Glioblastoma (GBM) is one of the most common primary malignant tumors in the central nervous system [ 1 ]. Despite continuous improvement in treatment, the prognosis of GBM remains poor due to the special location and high invasiveness [ 2 ], with a median survival of only 15 months. Vasculogenic mimicry (VM) is a new phenomenon about fluid-conducting channels discovered by Maniotis [ 3 ].…”

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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“…Brain glioma patients have a median survival time of less than 16 months after comprehensive treatment, which are mainly consisted of surgery, radiotherapy and chemotherapy [2]. However, the highly infiltrating property and the location of brain glioma make complete removal of the cancer cells impossible [3]. While radiotherapy applications are also limited by radiation-related encephalopathy.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of nanoscaled dual targeting drug-loaded liposomes on inhibiting vasculogenic mimicry channels of brain glioma

Xie

Zhan-Dui

Zhao

et al. 2021

Artificial Cells, Nanomedicine, and Biotechnology

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Brain glioma is the most common primary tumour of the central nervous system. Complete surgical removal of the brain glioma is virtually impossible. Chemotherapy is still an important treatment for brain glioma. However, blood-brain barrier (BBB) and vasculogenic mimicry (VM) channels remain two hindrances in regular treatments. Herein, we developed a novel nanoscaled dual targeting daunorubicin plus rofecoxib liposomes which could transport across the BBB, and eliminate brain glioma cells along with the VM channels. The liposomes were modified with two functional materials, and showed round in shape with a diameter about 120 nm. Evaluations were performed on human brain glioma U87MG cells in vitro and on intracranial brain glioma-bearing nude mice. The dual targeting liposomes demonstrated a long circulatory effect in the blood system, were able to transport across the BBB, and were accumulated into the brain. The results indicated that the dual targeting daunorubicin plus rofecoxib liposomes could inhibit the brain glioma VM channels and exhibited a significant efficacy in the treatment of intracranial glioma-bearing nude mice. The mechanisms are related to down regulations MMP-2, MMP-9, FAK and HIF-a. Hence, the established dual targeting liposomes could be a potential formulation to treat the brain glioma along with eliminating VM channels.

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C-type natriuretic peptide-modified lipid vesicles: fabrication and use for the treatment of brain glioma

Cited by 5 publications

References 51 publications

Dexamethasone increases production of C-type natriuretic peptide in the sheep brain

Dexamethasone increases production of C-type natriuretic peptide in the sheep brain

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

Evaluation of nanoscaled dual targeting drug-loaded liposomes on inhibiting vasculogenic mimicry channels of brain glioma

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