MAD2-p31comet axis deficiency reduces cell proliferation, migration and sensitivity of microtubule-interfering agents in glioma

Wu, Dang; Wang, Lepeng; Yang, Yanhong; Huang, Jin; Hu, Yuhua; Shu, Yongwei; Zhang, Jingyu; Zheng, Jing

doi:10.1016/j.bbrc.2018.02.011

Cited by 10 publications

(6 citation statements)

References 35 publications

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“…We found that Mad2 depletion in third-instar larval brains leads to increased aneuploidy, consistent with previous studies that have identified a role for Mad2 in neurological disease progression (Shi et al 2019 ; Wu et al 2018 ). Our findings align with studies in mammals, where aneuploidy has been implicated in neurodevelopmental disorders, including intellectual disabilities and autism spectrum disorders (Iourov et al 2006 ).…”

Section: Discussionsupporting

confidence: 92%

Aneuploidy is Linked to Neurological Phenotypes Through Oxidative Stress

Islam,

Shaukat,

Hussain

et al. 2024

J Mol Neurosci

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Aneuploidy, having an aberrant genome, is gaining increasing attention in neurodegenerative diseases. It gives rise to proteotoxic stress as well as a stereotypical oxidative shift which makes these cells sensitive to internal and environmental stresses. A growing body of research from numerous laboratories suggests that many neurodegenerative disorders, especially Alzheimer’s disease and frontotemporal dementia, are characterised by neuronal aneuploidy and the ensuing apoptosis, which may contribute to neuronal loss. Using Drosophila as a model, we investigated the effect of induced aneuploidy in GABAergic neurons. We found an increased proportion of aneuploidy due to Mad2 depletion in the third-instar larval brain and increased cell death. Depletion of Mad2 in GABAergic neurons also gave a defective climbing and seizure phenotype. Feeding animals an antioxidant rescued the climbing and seizure phenotype. These findings suggest that increased aneuploidy leads to higher oxidative stress in GABAergic neurons which causes cell death, climbing defects, and seizure phenotype. Antioxidant feeding represents a potential therapy to reduce the aneuploidy-driven neurological phenotype.

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Section: Discussionsupporting

confidence: 92%

Aneuploidy is Linked to Neurological Phenotypes Through Oxidative Stress

Islam,

Shaukat,

Hussain

et al. 2024

J Mol Neurosci

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“…Gliomas, the most common primary malignant brain tumor, show high recurrence and mortality rates 1 – 4 . Initially, they were categorized into grades I to IV based on the appearance of certain histopathologic characteristics, such as vascular proliferation, mitosis, polymorphism and necrosis 5 .…”

Section: Introductionmentioning

confidence: 99%

A new glioma grading model based on histopathology and Bone Morphogenetic Protein 2 mRNA expression

Zhou

Zhao

et al. 2020

Sci Rep

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Glioma, the most common form of primary malignant brain tumors, is graded based solely on histopathological appearance, which has led to prognostic discrepancies. This study aimed to establish a new glioma grading model by analyzing the expression of Bone Morphogenetic Protein 2 (BMP2) mRNA in patients with gliomas as well, named the Histopathological-BMP2 (HB) system. Clinical information was collected from 692 patients from the Chinese Glioma Genome Atlas database. According to pathological glioma subtypes and the expression of BMP2 mRNA in tumor tissues, the new subtypes HBs, HBh, HBm and HB1 were established, with BMP2 expression highest in HBs and lowest in HB1. Survival periods were analyzed. Based on this, the expression of three BMP2 receptors (BMPR1A, BMPR1B, and BMPR2) was also analyzed, which was related to the prognosis of patients. This new classification model was validated in further groups of patients from the CGGA database (n = 291) and the Cancer Genome Atlas (n = 625). A new glioma grade (HB grade) based on histopathology and BMP2 expression can predict the prognosis of glioma patients, with BMPR1B and BMPR2 expression indicating a different prognosis in different types of gliomas. The higher the concentration of BMP2, the better the prognosis of patients.

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“…Clinical therapy of glioma depends on the size, type, grade, and location of the tumor, as well as the age and overall health of the patient, and mainly consists of surgical resection followed by radiotherapy, chemotherapy, Chinese medicine treatment, gene therapy, and so on [3]. However, the mortality or recurrence of glioma is still high because of resistance to traditional chemotherapy [4], and the in-depth pathogenesis of glioma remains to be elaborated, including aberrant activation of proto-oncogenes and inactivation of tumor suppressors [5]. Therefore, it is of significant importance to enhance insights into the molecular mechanism and develop effective methods for the diagnosis and treatment of glioma.…”

Section: Introductionmentioning

confidence: 99%

LncRNA PVT1 Facilitates Tumorigenesis and Progression of Glioma via Regulation of MiR-128-3p/GREM1 Axis and BMP Signaling Pathway

Zhang

et al. 2018

Neurotherapeutics

133

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The current research was aimed at probing into the role of long noncoding RNA (lncRNA) PVT1 in the pathogenesis of glioma and the regulatory mechanism of PVT1/miR-128-3p/GREM1 network in glioma via regulation of the bone morphogenetic protein (BMP) signaling pathway. Microarray analysis was used for preliminary screening for candidate lncRNAs and mRNAs in glioma tissues. Real-time quantitative polymerase chain reaction, Western blot, MTT assay, flow cytometry, migration and invasion assays, and xenograft tumor model were utilized to examine the influence of the lncRNA PVT1/miR-128-3p/GREM1 network on the biological functions of glioma cells. Luciferase assay and RNA-binding protein immunoprecipitation assay were used to validate the miR-128-3p-target relationships with lncRNA PVT1 or GREM1. In addition, the impact of GREM1 on BMP signaling pathway downstream proteins BMP2 and BMP4 was detected via Western blot. LncRNA PVT1 was highly expressed in human glioma tissues and significantly associated with WHO grade (I-II vs III-IV; p < 0.05). There existed a regulatory relationship between lncRNA PVT1 and miR-128-3p as well as that between miR-128-3p and GREM1. MiR-128-3p was downregulated, whereas GREM1 was upregulated in glioma tissues in comparison with para-carcinoma tissues. Overexpression of GREM1 promoted the proliferation and metastatic potential of glioma cells, whereas miR-128-3p mimics inhibited the glioma cell activity through targeting GREM1. Furthermore, lncRNA PVT1 acted as a sponge of miR-128-3p and, thus, influenced the BMP signaling pathway downstream proteins BMP2 and BMP4 through regulating GREM1. LncRNA PVT1 modulated GREM1 and BMP downstream signaling proteins through sponging miR-128-3p, thereby promoting tumorigenesis and progression of glioma.

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MAD2-p31comet axis deficiency reduces cell proliferation, migration and sensitivity of microtubule-interfering agents in glioma

Cited by 10 publications

References 35 publications

Aneuploidy is Linked to Neurological Phenotypes Through Oxidative Stress

Aneuploidy is Linked to Neurological Phenotypes Through Oxidative Stress

A new glioma grading model based on histopathology and Bone Morphogenetic Protein 2 mRNA expression

LncRNA PVT1 Facilitates Tumorigenesis and Progression of Glioma via Regulation of MiR-128-3p/GREM1 Axis and BMP Signaling Pathway

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