Nanotechnology to augment immunotherapy for the treatment of glioblastoma multiforme

Ung, Nolan; Yang, Isaac

doi:10.1007/s11060-015-1814-1

Cited by 20 publications

(7 citation statements)

References 77 publications

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“…Various new treatment strategies, including immunotherapy, nanotechnology, and molecular-targeted therapy have emerged as potential therapeutic options. However, these treatment strategies still possess limited success and do not have a substantial clinical effect ( Polivka et al, 2012 ; Bambury and Morris, 2014 ; Ung and Yang, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Extracts of Artocarpus communis Induce Mitochondria-Associated Apoptosis via Pro-oxidative Activity in Human Glioblastoma Cells

et al. 2018

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Glioblastoma multiforme (GBM) is an extremely aggressive and devastating malignant tumor in the central nervous system. Its incidence is increasing and the prognosis is poor. Artocarpin is a natural prenylated flavonoid with various anti-inflammatory and anti-tumor properties. Studies have shown that artocarpin is associated with cell death of primary glioblastoma cells. However, the in vivo effects and the cellular and molecular mechanisms modulating the anticancer activities of artocarpin remain unknown. In this study, we demonstrated that treating the glioblastoma cell lines U87 and U118 cells with artocarpin induced apoptosis. Artocarpin-induced apoptosis is associated with caspase activation and poly (ADP-ribose) polymerase (PARP) cleavage and is mediated by the mitochondrial pathway. This is associated with mitochondrial depolarization, mitochondrial-derived reactive oxidative species (ROS) production, cytochrome c release, Bad and Bax upregulations, and Bcl-2 downregulation. Artocarpin induced NADPH oxidase/ROS generation plays an important role in the mitochondrial pathway activation. Furthermore, we found artocarpin-induced ROS production in mitochondria is associated with Akt- and ERK1/2 activation. After treatment with artocarpin, ROS causes PI3K/Akt/ERK1/2-induced cell death of these tumor cells. These observations were further verified by the results from the implantation of both U87 and U118 cells into in vivo mouse. In conclusion, our findings suggest that artocarpin induces mitochondria-associated apoptosis of glioma cells, suggesting that artocarpine can be a potential chemotherapeutic agent for future GBM treatment.

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Section: Introductionmentioning

confidence: 99%

Extracts of Artocarpus communis Induce Mitochondria-Associated Apoptosis via Pro-oxidative Activity in Human Glioblastoma Cells

et al. 2018

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“…Most of these have been administered systemically, and most frequently evaluated in melanoma or lymphoma tumor models. Immunotherapeutics for GBM treatment face the same physiological barriers that limit the effectiveness of standard therapy, as well as the added challenge of local immunosuppression present in the tumor microenvironment [84]. Nanocarriers offer a versatile platform to enhance the benefits of immunotherapy.…”

Section: Novel Therapeutic Agents For Treatment Of Brain Tumorsmentioning

confidence: 99%

Nanomaterials for convection-enhanced delivery of agents to treat brain tumors

Seo

Saltzman

2017

Current Opinion in Biomedical Engineering

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Nanomaterials represent a promising and versatile platform for the delivery of therapeutics to the brain. Treatment of brain tumors has been a long-standing challenge in the field of neuro-oncology. The current standard of care – a multimodal approach of surgery, radiation and chemotherapy – yields only a modest therapeutic benefit for patients with malignant gliomas. A major obstacle for treatment is the failure to achieve sufficient delivery of therapeutics at the tumor site. Recent advances in local drug delivery techniques, along with the development of highly effective brain-penetrating nanocarriers, have significantly improved treatment and imaging of brain tumors in preclinical studies. The major advantage of this combined strategy is the ability to optimize local therapy, by maintaining an effective and sustained concentration of therapeutics in the brain with minimal systemic toxicity. This review highlights some of the latest developments, significant advancements and current challenges in local delivery of nanomaterials for the treatment of brain tumors.

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“…Thus far, exposure to ionizing radiation is the only known risk factor for malignant gliomas [3]. For the most serious tumors of the nervous system, the current common treatment methods are surgery [4], chemotherapy [5], targeted therapy [6], and immunotherapy [7]. Despite these various treatment methods, the treatment effect and quality of life of glioma patients remain poor [8].…”

Section: Introductionmentioning

confidence: 99%

Transcription Factor FOXK1 Regulates the lncRNA NEAT1 to Promote Glioma Development Through Mediating KDM3A

Liu¹,

Wu²,

Wu³

et al. 2020

Preprint

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Background: Long noncoding RNAs are widely studied in glioma. However, the role of the lncRNA NEAT1 and KDM3A in glioma has not yet been reported. We aimed to reveal the role of these two lncRNAs in the development of glioma through this study.Methods: Samples from glioma patients and normal brain tissues were collected, and the expression of NEAT1 was detected by qRT-PCR. A dual-luciferase reporter gene assay, chromatin immunoprecipitation (ChIP), RNA-binding protein immunoprecipitation (RIP), and RNA pulldown experiments were used to identify the relationship between FOXK1, NEAT1, miR-128, and KDM3A. The CCK8 assay, Transwell assay and flow cytometry were used to detect cell viability, invasion and migration ability, and the cell cycle and apoptosis, respectively. Tumor formation experiments verified the effect of NEAT1 on gliomas in vivo.Results: FOXK1 and NEAT1 were significantly overexpressed in glioma tissues and cells, and NEAT1 was significantly related to WHO classification. FOXK1 bound the NEAT1 gene promoter region in glioma cells, and interference with FOXK1 inhibited NEAT1 expression. NEAT1 inhibited miR-128 expression by binding miR-128; significantly improved cell viability and invasion and migration capabilities; increased the expression of KDM3A and activated the Wnt signaling pathway. Interference with KDM3A reversed the above results. In addition, interference with NEAT1 decreased KDM3A expression and inhibited tumor growth.Conclusion: Interference with NEAT1 promoted the expression of miR-128, thereby suppressing the expression of KDM3A and inhibiting the occurrence and development of glioma, while the expression of NEAT1 was shown to be regulated by the upstream transcription factor FOXK1.

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Nanotechnology to augment immunotherapy for the treatment of glioblastoma multiforme

Cited by 20 publications

References 77 publications

Extracts of Artocarpus communis Induce Mitochondria-Associated Apoptosis via Pro-oxidative Activity in Human Glioblastoma Cells

Extracts of Artocarpus communis Induce Mitochondria-Associated Apoptosis via Pro-oxidative Activity in Human Glioblastoma Cells

Nanomaterials for convection-enhanced delivery of agents to treat brain tumors

Transcription Factor FOXK1 Regulates the lncRNA NEAT1 to Promote Glioma Development Through Mediating KDM3A

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