The Glycoprotein M6a Is Associated with Invasiveness and Radioresistance of Glioblastoma Stem Cells

Lacore, Marie Géraldine; Delmas, Caroline; Nicaise, Yvan; Kowalski‐Chauvel, Aline; Cohen-Jonathan-Moyal, Elizabeth; Seva, Catherine

doi:10.3390/cells11142128

Cited by 8 publications

(7 citation statements)

References 33 publications

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“…GPM6A expression is restricted to neurons, while GPM6B is expressed in both neurons and glia 19 . In normal neuronal cells, GPM6A accumulates in lipid raft domains and acts as a transducer of extracellular signals such as laminins 20 . It plays an essential role in neurite outgrowth, filopodia formation, and neuronal migration.…”

Section: Discussionmentioning

confidence: 99%

Glycoprotein M6A upregulation detected by transcriptome analysis controls the proliferation of keloidal fibroblasts

Kurimoto‐Nishiguchi,

Muraoka,

Inaba

et al. 2023

The Journal of Dermatology

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Hypertrophic scars and keloids are fibroproliferative disorders caused by abnormal wound healing. Their exact cause has not been found, but abnormalities during the wound healing process including inflammatory, immune, genetic, and other factors are thought to predispose an individual to excessive scarring. In the present study, we performed transcriptome analysis of established keloid cell lines (KEL FIB), focusing on gene expression analysis and fusion gene detection for the first time. For gene expression analysis, fragments per kilobase per million map read values were calculated, which were validated by real‐time PCR and immunohistochemistry. Fusion genes were predicted by transcriptome sequence, and validated by Sanger sequence and G‐banding. As a result, GPM6A was shown in the expression analysis to be upregulated in KEL FIB compared with normal fibroblasts. The GPM6A upregulation in KEL FIB was confirmed by real‐time PCR, and GPM6A messenger ribonucleic acid expression was consistently significantly elevated in the tissues of hypertrophic scar and keloid compared to normal skin. Immunohistochemistry also revealed that the number of fibroblast‐like spindle‐shaped cells positive for GPM6A was significantly increased in keloidal tissues. GPM6A inhibition by small interfering ribonucleic acid significantly reduced the number of KEL FIB. On the other hand, although we hypothesized that fusion genes are involved in the pathogenesis of keloids, the transcriptome analysis could not prove the presence of fusion genes in KEL FIB. Taken together, GPM6A upregulation may have an inducible effect on cell proliferation in keloidal fibroblasts. GPM6A can be a novel therapeutic target in hypertrophic scars and keloids. The inflammatory nature may be more prominent in the pathogenesis of keloids, rather than being skin tumors, as proposed by Ogawa et al. Future studies using several cell lines will be required.

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Section: Discussionmentioning

confidence: 99%

Glycoprotein M6A upregulation detected by transcriptome analysis controls the proliferation of keloidal fibroblasts

Kurimoto‐Nishiguchi,

Muraoka,

Inaba

et al. 2023

The Journal of Dermatology

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“…This test, which is the most used for the evaluation of the response to ionizing radiation, provide experimental survival curves representing the survival fraction (SF) as a function of radiation dose ( 44 ). Although the ability of SF2 to predict the clinical response of human HGG to radiotherapy has not been demonstrated ( 45 , 46 ), this parameter is widely used to compare the radiosensitivity of different cancer cell lines or to assess the radiosensitizing potential of new therapeutics in vitro ( 47 , 48 ). As it takes into account the entire survival curve, MID is also a useful parameter for quantifying differences in survival curves between cell lines.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of in vitro intrinsic radiosensitivity and characterization of five canine high-grade glioma cell lines

Cartiaux,

Deviers,

Delmas

et al. 2023

Front. Vet. Sci.

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Glioma is the most common primary brain tumor in dogs and predominantly affects brachycephalic breeds. Diagnosis relies on CT or MRI imaging, and the proposed treatments include surgical resection, chemotherapy, and radiotherapy depending on the tumor’s location. Canine glioma from domestic dogs could be used as a more powerful model to study radiotherapy for human glioma than the murine model. Indeed, (i) contrary to mice, immunocompetent dogs develop spontaneous glioma, (ii) the canine brain structure is closer to human than mice, and (iii) domestic dogs are exposed to the same environmental factors than humans. Moreover, imaging techniques and radiation therapy used in human medicine can be applied to dogs, facilitating the direct transposition of results. The objective of this study is to fully characterize 5 canine glioma cell lines and to evaluate their intrinsic radiosensitivity. Canine cell lines present numerous analogies between the data obtained during this study on different glioma cell lines in dogs. Cell morphology is identical, such as doubling time, clonality test and karyotype. Immunohistochemical study of surface proteins, directly on cell lines and after stereotaxic injection in mice also reveals close similarity. Radiosensitivity profile of canine glial cells present high profile of radioresistance.

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“…PTPRZ1 expression in GBM stem cells was shown to be upregulated by HOXA5 and contribute to cell survival and a worse GBM outcome [21]. Preferential PTPRZ1 expression in GBM stem cells correlates with that of the glycoprotein M6a (GPM6A) and targeting either of these molecules inhibited the invasive and sphere-forming ability of these cells and enhanced their sensitivity to radiation [80].…”

Section: Ptprz1 In Cancermentioning

confidence: 99%

Protein Tyrosine Phosphatase Receptor Zeta 1 as a Potential Target in Cancer Therapy and Diagnosis

Papadimitriou

Kanellopoulou

2023

IJMS

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Protein tyrosine phosphatase receptor zeta 1 (PTPRZ1) is a type V transmembrane tyrosine phosphatase that is highly expressed during embryonic development, while its expression during adulthood is limited. PTPRZ1 is highly detected in the central nervous system, affecting oligodendrocytes’ survival and maturation. In gliomas, PTPRZ1 expression is significantly upregulated and is being studied as a potential cancer driver and as a target for therapy. PTPRZ1 expression is also increased in other cancer types, but there are no data on the potential functional significance of this finding. On the other hand, low PTPRZ1 expression seems to be related to a worse prognosis in some cancer types, suggesting that in some cases, it may act as a tumor-suppressor gene. These discrepancies may be due to our limited understanding of PTPRZ1 signaling and tumor microenvironments. In this review, we present evidence on the role of PTPRZ1 in angiogenesis and cancer and discuss the phenomenal differences among the different types of cancer, depending on the regulation of its tyrosine phosphatase activity or ligand binding. Clarifying the involved signaling pathways will lead to its efficient exploitation as a novel therapeutic target or as a biomarker, and the development of proper therapeutic approaches.

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The Glycoprotein M6a Is Associated with Invasiveness and Radioresistance of Glioblastoma Stem Cells

Cited by 8 publications

References 33 publications

Glycoprotein M6A upregulation detected by transcriptome analysis controls the proliferation of keloidal fibroblasts

Glycoprotein M6A upregulation detected by transcriptome analysis controls the proliferation of keloidal fibroblasts

Evaluation of in vitro intrinsic radiosensitivity and characterization of five canine high-grade glioma cell lines

Protein Tyrosine Phosphatase Receptor Zeta 1 as a Potential Target in Cancer Therapy and Diagnosis

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