Tenascin C promotes cancer cell plasticity in mesenchymal glioblastoma

Angel, Inbar; Kerman, Ori Pilo; Rousso-Noori, Liat; Friedmann‐Morvinski, Dinorah

doi:10.1038/s41388-020-01506-6

Cited by 39 publications

(43 citation statements)

References 51 publications

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“…Under hypoxic conditions, 005 GSCs have the capacity to transdifferentiate and give rise to TDEC both in vitro (Fig. 5a ) and in vivo 34 , 35 . Confocal microscopy (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Hyaluronic acid (HA) is an important component of the brain extracellular matrix (ECM) and is one of the major components of GBM-ECM. In addition to anatomical and physical aspects, specific ECM components in GBM, such as Tenascin C, fibronectin, and hyaluronan were shown to contribute in different aspects of tumor biology (e.g., invasiveness, proliferation, angiogenesis) 35 . Based on a recently reported study 41 , we speculate that increased levels of HA may disrupt the normal localization of p32 in the mitochondria and induce its translocation to the cell surface.…”

Section: Discussionmentioning

confidence: 99%

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P32-specific CAR T cells with dual antitumor and antiangiogenic therapeutic potential in gliomas

et al. 2021

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Glioblastoma is considered one of the most aggressive malignancies in adult and pediatric patients. Despite decades of research no curative treatment is available and it thus remains associated with a very dismal prognosis. Although recent pre-clinical and clinical studies have demonstrated the feasibility of chimeric antigen receptors (CAR) T cell immunotherapeutic approach in glioblastoma, tumor heterogeneity and antigen loss remain among one of the most important challenges to be addressed. In this study, we identify p32/gC1qR/HABP/C1qBP to be specifically expressed on the surface of glioma cells, making it a suitable tumor associated antigen for redirected CAR T cell therapy. We generate p32 CAR T cells and find them to recognize and specifically eliminate p32 expressing glioma cells and tumor derived endothelial cells in vitro and to control tumor growth in orthotopic syngeneic and xenograft mouse models. Thus, p32 CAR T cells may serve as a therapeutic option for glioblastoma patients.

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“…Under hypoxic conditions, 005 GSCs have the capacity to transdifferentiate and give rise to TDEC both in vitro (Fig. 5a ) and in vivo 34 , 35 . Confocal microscopy (Fig.…”

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

P32-specific CAR T cells with dual antitumor and antiangiogenic therapeutic potential in gliomas

et al. 2021

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“…Tenascin-C also promotes invasion of brain tumor-initiating cells, which is regulated by metalloproteinase ADAM-9 ( Sarkar et al, 2015 ). Consistently, shRNA designed for targeting TN-C impairs glioma cell motility in wound-scratch assay ( Angel et al, 2020 ). It has been suggested that Tenascin-R (TN-R) and Tenascin-W (TN-W), as members of the tenascin family, may be associated with progression and malignancy of glioma cells; however, that hypothesis remains to be elucidated.…”

Section: The Interaction Between the Extracellular Matrix And Binding Proteins For Migrationmentioning

confidence: 94%

Mechanisms of Invasion in Glioblastoma: Extracellular Matrix, Ca2+ Signaling, and Glutamate

Kim

Han

2021

Front. Cell. Neurosci.

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Glioblastoma (GBM) is the most common and malignant form of primary brain tumor with a median survival time of 14–16 months in GBM patients. Surgical treatment with chemotherapy and radiotherapy may help increase survival by removing GBM from the brain. However, complete surgical resection to eliminate GBM is almost impossible due to its high invasiveness. When GBM cells migrate to the brain, they interact with various cells, including astrocytes, neurons, endothelial cells, and the extracellular matrix (ECM). They can also make their cell body shrink to infiltrate into narrow spaces in the brain; thereby, they can invade regions of the brain and escape from surgery. Brain tumor cells create an appropriate microenvironment for migration and invasion by modifying and degrading the ECM. During those processes, the Ca2+ signaling pathway and other signaling cascades mediated by various ion channels contribute mainly to gene expression, motility, and invasion of GBM cells. Furthermore, GBM cells release glutamate, affecting migration via activation of ionotropic glutamate receptors in an autocrine manner. This review focuses on the cellular mechanisms of glioblastoma invasion and motility related to ECM, Ca2+ signaling, and glutamate. Finally, we discuss possible therapeutic interventions to inhibit invasion by GBM cells.

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“…TNC is a high molecular weight glycoprotein that plays an ECM to stabilize the basement membrane with collagen. Interestingly, TNC is reportedly induced by obesity-related inflammatory responses in the adipose tissue [26] and tumor microenvironment [27]. Tenascin has four isoforms, TNC, TNR, TNXB, and TNW, in cattle.…”

Section: Discussionmentioning

confidence: 99%

Gene Expression Analysis Provides New Insights into the Mechanism of Intramuscular Fat Formation in Japanese Black Cattle

Ueda

Hosoda

Yoshino

et al. 2021

Genes

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Japanese Black cattle (Japanese Wagyu) have a unique phenotype in which ectopic intramuscular fat accumulates in skeletal muscle, producing finely marbled beef. However, the mechanism of intramuscular fat formation in Japanese Black cattle remains unclear. To investigate the key genes involved in intramuscular fat accumulation, we comprehensively analyzed mRNA levels in subcutaneous and intramuscular fat tissues using RNA sequence (RNA-seq) analysis, which detected 27,606 genes. We identified eight key genes, namely carboxypeptidase E, tenascin C, transgelin, collagen type IV alpha 5 (COL4A5), cysteine and glycine-rich protein 2, PDZ, and LIM domain 3, phosphatase 1 regulatory inhibitor subunit 14A, and regulator of calcineurin 2. These genes were highly and specifically expressed in intramuscular fat tissue. Immunohistochemical analysis revealed a collagen network, including COL4A5, in the basement membrane around the intramuscular fat tissue. Moreover, pathway analysis revealed that, in intramuscular fat tissue, differentially expressed genes are related to cell adhesion, proliferation, and cancer pathways. Furthermore, pathway analysis showed that the transforming growth factor-β (TGF-β) and small GTPases regulators RASGRP3, ARHGEF26, ARHGAP10, ARHGAP24, and DLC were upregulated in intramuscular fat. Our study suggests that these genes are involved in intramuscular fat formation in Japanese Black cattle.

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Tenascin C promotes cancer cell plasticity in mesenchymal glioblastoma

Cited by 39 publications

References 51 publications

P32-specific CAR T cells with dual antitumor and antiangiogenic therapeutic potential in gliomas

P32-specific CAR T cells with dual antitumor and antiangiogenic therapeutic potential in gliomas

Mechanisms of Invasion in Glioblastoma: Extracellular Matrix, Ca2+ Signaling, and Glutamate

Gene Expression Analysis Provides New Insights into the Mechanism of Intramuscular Fat Formation in Japanese Black Cattle

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