Combined-therapeutic strategies synergistically potentiate glioblastoma multiforme treatment <i>via</i> nanotechnology

Yang, Jun; Shi, Zhuyan; Liu, Ruiyuan; Wu, Yanyue; Zhang, Xin

doi:10.7150/thno.40298

Cited by 76 publications

(51 citation statements)

References 163 publications

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“…Glioblastoma (GBM) is one of the most aggressive tumors in central nervous system [1] with a median overall survival less than 15 months due to the very nature of GBM [2]. The current standard strategy of GBM including maximum safe resection, radiotherapy and the temozolomide (TMZ) chemotherapy are widely applied, however, most GBM patients still develop rapid tumor recurrence within a period of 7 months [3].…”

Section: Introductionmentioning

confidence: 99%

Loss of PLK2 induces acquired resistance to temozolomide in GBM via activation of notch signaling

Wahafu

et al. 2020

J Exp Clin Cancer Res

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Background Glioblastoma (GBM) is a lethal type of primary brain tumor with a median survival less than 15 months. Despite the recent improvements of comprehensive strategies, the outcomes for GBM patients remain dismal. Accumulating evidence indicates that rapid acquired chemoresistance is the major cause of GBM recurrence thus leads to worse clinical outcomes. Therefore, developing novel biomarkers and therapeutic targets for chemoresistant GBM is crucial for long-term cures. Methods Transcriptomic profiles of glioblastoma were downloaded from gene expression omnibus (GEO) and TCGA database. Differentially expressed genes were analyzed and candidate gene PLK2 was selected for subsequent validation. Clinical samples and corresponding data were collected from our center and measured using immunohistochemistry analysis. Lentiviral transduction and in vivo xenograft transplantation were used to validate the bioinformatic findings. GSEA analyses were conducted to identify potential signaling pathways related to PLK2 expression and further confirmed by in vitro mechanistic assays. Results In this study, we identified PLK2 as an extremely suppressed kinase-encoding gene in GBM samples, particularly in therapy resistant GBM. Additionally, reduced PLK2 expression implied poor prognosis and TMZ resistance in GBM patients. Functionally, up-regulated PLK2 attenuated cell proliferation, migration, invasion, and tumorigenesis of GBM cells. Besides, exogenous overexpression of PLK2 reduced acquired TMZ resistance of GBM cells. Furthermore, bioinformatics analysis indicated that PLK2 was negatively correlated with Notch signaling pathway in GBM. Mechanically, loss of PLK2 activated Notch pathway through negative transcriptional regulation of HES1 and degradation of Notch1. Conclusion Loss of PLK2 enhances aggressive biological behavior of GBM through activation of Notch signaling, indicating that PLK2 could be a prognostic biomarker and potential therapeutic target for chemoresistant GBM.

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Section: Introductionmentioning

confidence: 99%

Loss of PLK2 induces acquired resistance to temozolomide in GBM via activation of notch signaling

Wahafu

et al. 2020

J Exp Clin Cancer Res

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“…Known as a very aggressive brain cancer, it is one of the most lethal malignancies in humans [ 1 , 2 ]. At present, the prognosis of patients with GBM remains very poor, with a median survival time of 15 months [ 3 , 4 ]. Therefore, an in-depth investigation of the molecular mechanisms underlying the development of GBM is conducive to advances in GBM diagnosis and treatment.…”

Section: Introductionmentioning

confidence: 99%

AEBP1 Promotes Glioblastoma Progression and Activates the Classical NF-κB Pathway

Guo

Song

Chang

et al. 2020

Behavioural Neurology

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Objective. Our study was aimed at investigating the mechanistic consequences of the upregulation of adipocyte enhancer-binding protein 1 (AEBP1) in glioblastoma (GBM). Methods. The expression of AEBP1 in GBM was assessed by bioinformatics analysis and qRT-PCR; the effects of AEBP1 on GBM cell proliferation, migration, invasion, and tumor growth in vitro and in vivo were detected by a CCK-8 assay, colony formation assay, scratch assay, Transwell assay, and subcutaneous tumor formation, respectively. The activation of related signaling pathways was monitored using western blot. Results. Tumor-related databases and bioinformatics analysis revealed that AEBP1 was highly expressed in GBM and indicated poor outcome of patients; its high expression that was also confirmed in GBM tissues and cell lines was closely related to the tumor size. The results of in vitro experiments showed that AEBP1 could significantly promote GBM cell proliferation, migration, and invasion; in vivo experiments suggested that AEBP1 could contribute to the growth of GBM tumors. AEBP1 could upregulate the level of IκBα phosphorylation, decrease IκBα expression, activate the NF-κB signaling pathway, and promote the expression of downstream oncogenes. Conclusion. Upregulated AEBP1 in GBM promotes GBM cell proliferation, migration, and invasion and facilitates tumor growth in vivo by activating the classical NF-κB pathway.

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“…Similarly, the combination of photoimmunotherapy exhibited a better effect compared to either phototherapy or immunotherapy against brain cancer. The combination therapy uses the specific antibodies that could facilitate targeting the tumor cells without damaging the normal cells and also uses enhanced photosensitizer delivery into tumors and increases the light-activated cytotoxicity [173]. Recently, gene therapy was used as an adjuvant for the current glioblastoma treatments.…”

Section: Cns Cancersmentioning

confidence: 99%

Role and Therapeutic Potential of Melatonin in the Central Nervous System and Cancers

Gurunathan

Kang

Kim

2020

Cancers

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Melatonin (MLT) is a powerful chronobiotic hormone that controls a multitude of circadian rhythms at several levels and, in recent times, has garnered considerable attention both from academia and industry. In several studies, MLT has been discussed as a potent neuroprotectant, anti-apoptotic, anti-inflammatory, and antioxidative agent with no serious undesired side effects. These characteristics raise hopes that it could be used in humans for central nervous system (CNS)-related disorders. MLT is mainly secreted in the mammalian pineal gland during the dark phase, and it is associated with circadian rhythms. However, the production of MLT is not only restricted to the pineal gland; it also occurs in the retina, Harderian glands, gut, ovary, testes, bone marrow, and lens. Although most studies are limited to investigating the role of MLT in the CNS and related disorders, we explored a considerable amount of the existing literature. The objectives of this comprehensive review were to evaluate the impact of MLT on the CNS from the published literature, specifically to address the biological functions and potential mechanism of action of MLT in the CNS. We document the effectiveness of MLT in various animal models of brain injury and its curative effects in humans. Furthermore, this review discusses the synthesis, biology, function, and role of MLT in brain damage, and as a neuroprotective, antioxidative, anti-inflammatory, and anticancer agent through a collection of experimental evidence. Finally, it focuses on the effect of MLT on several neurological diseases, particularly CNS-related injuries.

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Combined-therapeutic strategies synergistically potentiate glioblastoma multiforme treatment via nanotechnology

Cited by 76 publications

References 163 publications

Loss of PLK2 induces acquired resistance to temozolomide in GBM via activation of notch signaling

Loss of PLK2 induces acquired resistance to temozolomide in GBM via activation of notch signaling

AEBP1 Promotes Glioblastoma Progression and Activates the Classical NF-κB Pathway

Role and Therapeutic Potential of Melatonin in the Central Nervous System and Cancers

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