Hypoxia, Angiogenesis and Mechanisms for Invasion of Malignant Gliomas

Province, Paula; Griguer, Corinne E.; Han, Xiaosi; Louis, B Nabors; Shaykh, Hassan F

doi:10.5772/53298

Cited by 8 publications

(13 citation statements)

References 87 publications

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“…Many processes that involve cellular invasion, blastocyst implantation, placental development, and also rapidly growing tumors occur under reduced oxygen environments [ 21 ]. The dynamic and multifactorial process of hypoxia also activates signaling pathways leading to angiogenesis, enhanced motility/invasion, changes in metabolism, and the ability to survive to oxidative stress [ 22 ]. Hypoxia is known to increase the metastatic and angiogenic potential of tumor cells and has been associated with increased metastasis and poor prognosis in patients with different types of cancer [ 22 – 25 ].…”

Section: Introductionmentioning

confidence: 99%

“…The dynamic and multifactorial process of hypoxia also activates signaling pathways leading to angiogenesis, enhanced motility/invasion, changes in metabolism, and the ability to survive to oxidative stress [ 22 ]. Hypoxia is known to increase the metastatic and angiogenic potential of tumor cells and has been associated with increased metastasis and poor prognosis in patients with different types of cancer [ 22 – 25 ]. Tumor cells are characterized by high proliferation rates finally resulting in structural and functional abnormal blood vessels unable to provide an adequate amount of oxygen to sustain the increased metabolic demands of cell growth, which ultimately results in hypoxia [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

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Hypoxic Modulation of HLA-G Expression through the Metabolic Sensor HIF-1 in Human Cancer Cells

Garziera

Scarabel

Toffoli

2017

Journal of Immunology Research

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The human leukocyte antigen-G (HLA-G) is considered an immune checkpoint molecule involved in tumor immune evasion. Hypoxia and the metabolic sensor hypoxia-inducible factor 1 (HIF-1) are hallmarks of metastasization, angiogenesis, and intense tumor metabolic activity. The purpose of this review was to examine original in vitro studies carried out in human cancer cell lines, which reported data about HLA-G expression and HIF-1 mediated-HLA-G expression in response to hypoxia. The impact of HLA-G genomic variability on the hypoxia responsive elements (HREs) specific for HIF-1 binding was also discussed. Under hypoxia, HLA-G-negative cell lines might transcribe HLA-G without translation of the protein while in contrast, HLA-G-positive cell lines, showed a reduced HLA-G transcriptional activity and protein level. HIF-1 modulation of HLA-G expression induced by hypoxia was demonstrated in different cell lines. HLA-G SNPs rs1632947 and rs41551813 located in distinct HREs demonstrated a prominent role of HIF-1 binding by DNA looping. Our research revealed a fine regulation of HLA-G in hypoxic conditions through HIF-1, depending on the cellular type and HLA-G genomic variability. Specifically, SNPs found in HREs should be considered in future investigations as markers with potential clinical value especially in metastatic malignancies.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hypoxic Modulation of HLA-G Expression through the Metabolic Sensor HIF-1 in Human Cancer Cells

Garziera

Scarabel

Toffoli

2017

Journal of Immunology Research

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“…The inhibition of intracellular ROS production and/or intensification of ROS clearance are considered necessary to promote cell survival during and after oxidative stress [ 26 ]. Rapidly expanding tumors, e.g., glioblastomas, are characterized by a fluctuating availability of oxygen and nutrients such as glucose, and malignant progression is supposed to arise from the adaptation to these conditions [ 27 ]. In order to mimic that situation, we subjected the cells to serum, glucose, and oxygen restriction.…”

Section: Resultsmentioning

confidence: 99%

Knockdown of the TP53-Induced Glycolysis and Apoptosis Regulator (TIGAR) Sensitizes Glioma Cells to Hypoxia, Irradiation and Temozolomide

Maurer

Heller

Wanka

et al. 2019

IJMS

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The TP53-induced glycolysis and apoptosis regulator (TIGAR) has been shown to decrease glycolysis, to activate the pentose phosphate pathway, and to provide protection against oxidative damage. Hypoxic regions are considered characteristic of glioblastoma and linked with resistance to current treatment strategies. Here, we established that LNT-229 glioma cell lines stably expressed shRNA constructs targeting TIGAR, and exposed them to hypoxia, irradiation and temozolomide. The disruption of TIGAR enhanced levels of reactive oxygen species and cell death under hypoxic conditions, as well as the effectiveness of irradiation and temozolomide. In addition, TIGAR was upregulated by HIF-1α. As a component of a complex network, TIGAR contributes to the metabolic adjustments that arise from either spontaneous or therapy-induced changes in tumor microenvironment.

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“…In this review, we summarise recent advances relating to the biological consequence and therapeutic efficacy of tumour hypoxia [13,14]. We outline the negative impact of tumour hypoxia on the propagation of cancer stem cells, malignant progression, metastasis immunosuppression and metabolic reprogramming.…”

Section: Scope Of the Reviewmentioning

confidence: 99%

Exploiting Current Understanding of Hypoxia Mediated Tumour Progression for Nanotherapeutic Development

Feng

Byrne

Jamal

et al. 2019

Cancers

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Hypoxia is one of the most common phenotypes of malignant tumours. Hypoxia leads to the increased activity of hypoxia-inducible factors (HIFs), which regulate the expression of genes controlling a raft of pro-tumour phenotypes. These include maintenance of the cancer stem cell compartment, epithelial-mesenchymal transition (EMT), angiogenesis, immunosuppression, and metabolic reprogramming. Hypoxia can also contribute to the tumour progression in a HIF-independent manner via the activation of a complex signalling network pathway, including JAK-STAT, RhoA/ROCK, NF-κB and PI3/AKT. Recent studies suggest that nanotherapeutics offer a unique opportunity to target the hypoxic microenvironment, enhancing the therapeutic window of conventional therapeutics. In this review, we summarise recent advances in understanding the impact of hypoxia on tumour progression, while outlining possible nanotherapeutic approaches for overcoming hypoxia-mediated resistance.

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Hypoxia, Angiogenesis and Mechanisms for Invasion of Malignant Gliomas

Cited by 8 publications

References 87 publications

Hypoxic Modulation of HLA-G Expression through the Metabolic Sensor HIF-1 in Human Cancer Cells

Hypoxic Modulation of HLA-G Expression through the Metabolic Sensor HIF-1 in Human Cancer Cells

Knockdown of the TP53-Induced Glycolysis and Apoptosis Regulator (TIGAR) Sensitizes Glioma Cells to Hypoxia, Irradiation and Temozolomide

Exploiting Current Understanding of Hypoxia Mediated Tumour Progression for Nanotherapeutic Development

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