Tumor-associated mesenchymal stem-like cells provide extracellular signaling cue for invasiveness of glioblastoma cells

Lim, Eun Jung; Suh, Yongjoon; Yoo, Kyoungkeun; Lee, Ji Hyun; Kim, In Gyu; Kim, Min Jung; Chang, Jong Hee; Kang, Seok‐Gu; Lee, Su Jae

doi:10.18632/oncotarget.13638

Cited by 32 publications

(26 citation statements)

References 36 publications

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“…108 In other studies, MSC-like cells were isolated from the GB tumor core and shown to increase angiogenesis, GB cell proliferation, and invasion. [110][111][112][113][114] Consistent with these findings, the percentage of GB-associated MSC-like cells has recently been shown to be inversely correlated with overall survival, indicating a role for these cells in promoting the aggressive behavior of GB. 115,116 All these data raise questions about the suitability of MSCs as cellular vehicles for the delivery of therapeutic molecules in the context of GB.…”

Section: Adult Stem Cellssupporting

confidence: 55%

<p>Nanocarriers and nonviral methods for delivering antiangiogenic factors for glioblastoma therapy: the story so far</p>

Clavreul¹,

Pourbaghi-Masouleh²,

Roger³

et al. 2019

IJN

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Angiogenesis, the formation of new blood vessels, is an essential component of glioblastoma (GB) progression. The development of angiogenesis inhibitor therapy, including treatments targeting vascular endothelial growth factor (VEGF) in particular, raised new hopes for the treatment of GB, but no Phase III clinical trial to date has reported survival benefits relative to standard treatment. There are several possible reasons for this limited efficacy, including VEGF-independent angiogenesis, induction of tumor invasion, and inefficient antiangiogenic factor delivery to the tumor. Efforts have been made to overcome these limitations by identifying new angiogenesis inhibitors that target angiogenesis through different mechanisms of action without inducing tumor invasion, and through the development of viral and nonviral delivery methods to improve antiangiogenic activity. Herein, we describe the nonviral methods, including convection-enhanced delivery devices, implantable polymer devices, nanocarriers, and cellular vehicles, to deliver antiangiogenic factors. We focus on those evaluated in intracranial (orthotopic) animal models of GB, the most relevant models of this disease, as they reproduce the clinical scenario of tumor progression and therapy response encountered in GB patients.

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Section: Adult Stem Cellssupporting

confidence: 55%

<p>Nanocarriers and nonviral methods for delivering antiangiogenic factors for glioblastoma therapy: the story so far</p>

Clavreul¹,

Pourbaghi-Masouleh²,

Roger³

et al. 2019

IJN

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“…Importantly, HA is found to be more abundant in the peritumoral regions compared to distant normal brain tissue [ 250 ]. A recent study by Lim et al suggests that tumor-associated mesenchymal stem-like cells—stromal cells that interact with glioma cells—may contribute to the high abundance of HA in the tumor microenvironment through the induction of HA synthase-2 [ 251 ]. Apart from providing mechanical support, HA interacts with multiple cognate receptors—including CD44, receptor for hyaluronate-mediated motility (RHAMM), and intercellular adhesion molecule-1 (ICAM-1)—whose elevated expression correlate with worse patient prognosis in GBM [ 252 ].…”

Section: Paving the Way For Invasion: How Glioma Cells Remodel The Ecmentioning

confidence: 99%

Developmentally regulated signaling pathways in glioma invasion

Mehta

Cascio

2017

Cell. Mol. Life Sci.

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Malignant gliomas are the most common, infiltrative, and lethal primary brain tumors affecting the adult population. The grim prognosis for this disease is due to a combination of the presence of highly invasive tumor cells that escape surgical resection and the presence of a population of therapy-resistant cancer stem cells found within these tumors. Several studies suggest that glioma cells have cleverly hijacked the normal developmental program of neural progenitor cells, including their transcriptional programs, to enhance gliomagenesis. In this review, we summarize the role of developmentally regulated signaling pathways that have been found to facilitate glioma growth and invasion. Furthermore, we discuss how the microenvironment and treatment-induced perturbations of these highly interconnected signaling networks can trigger a shift in cellular phenotype and tumor subtype.

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“…However, with remarkable advancement in technology and analytical methods seen in the last decade, attention has shifted to the TM contribution towards the development of chemoresistance [ 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 ]. Chemotherapeutic drugs need to access all cancer cells in a solid tumor to be effective, thus components of the tumor microenvironment become important players in the response of these cells to drugs [ 33 , 47 , 48 , 49 , 50 , 51 , 52 , 53 ]. The TM is a dynamic entity and is characterized by cellular heterogeneous, the amounts of oxygen, nutrients and ECM proteins [ 41 , 54 , 55 , 56 , 57 , 58 , 59 ].…”

Section: Introductionmentioning

confidence: 99%

The Role of Tumor Microenvironment in Chemoresistance: To Survive, Keep Your Enemies Closer

Senthebane

Rowe

Thomford

et al. 2017

IJMS

314

305

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Chemoresistance is a leading cause of morbidity and mortality in cancer and it continues to be a challenge in cancer treatment. Chemoresistance is influenced by genetic and epigenetic alterations which affect drug uptake, metabolism and export of drugs at the cellular levels. While most research has focused on tumor cell autonomous mechanisms of chemoresistance, the tumor microenvironment has emerged as a key player in the development of chemoresistance and in malignant progression, thereby influencing the development of novel therapies in clinical oncology. It is not surprising that the study of the tumor microenvironment is now considered to be as important as the study of tumor cells. Recent advances in technological and analytical methods, especially ‘omics’ technologies, has made it possible to identify specific targets in tumor cells and within the tumor microenvironment to eradicate cancer. Tumors need constant support from previously ‘unsupportive’ microenvironments. Novel therapeutic strategies that inhibit such microenvironmental support to tumor cells would reduce chemoresistance and tumor relapse. Such strategies can target stromal cells, proteins released by stromal cells and non-cellular components such as the extracellular matrix (ECM) within the tumor microenvironment. Novel in vitro tumor biology models that recapitulate the in vivo tumor microenvironment such as multicellular tumor spheroids, biomimetic scaffolds and tumor organoids are being developed and are increasing our understanding of cancer cell-microenvironment interactions. This review offers an analysis of recent developments on the role of the tumor microenvironment in the development of chemoresistance and the strategies to overcome microenvironment-mediated chemoresistance. We propose a systematic analysis of the relationship between tumor cells and their respective tumor microenvironments and our data show that, to survive, cancer cells interact closely with tumor microenvironment components such as mesenchymal stem cells and the extracellular matrix.

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Tumor-associated mesenchymal stem-like cells provide extracellular signaling cue for invasiveness of glioblastoma cells

Cited by 32 publications

References 36 publications

<p>Nanocarriers and nonviral methods for delivering antiangiogenic factors for glioblastoma therapy: the story so far</p>

<p>Nanocarriers and nonviral methods for delivering antiangiogenic factors for glioblastoma therapy: the story so far</p>

Developmentally regulated signaling pathways in glioma invasion

The Role of Tumor Microenvironment in Chemoresistance: To Survive, Keep Your Enemies Closer

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