Glioblastoma stem cell-specific histamine secretion drives pro-angiogenic tumor microenvironment remodeling

Chen, Jiayi; Liu, Guangqin; Wang, Xinzheng; Hong, Huasheng; Li, Tingting; Li, Lin; Wang, Hongxiang; Xie, Jiong; Li, Bohan; Li, Ting; Lu, Dingyi; Zhang, Yakun; Zhao, Hongbo; Yao, Chengcheng; Wen, Kaiqing; Li, Teng; Chen, Jing; Wu, Shengming; He, Kun; Zhang, Weina; Zhao, Jie; Wang, Na; Han, Qin; Xia, Qing; Qi, Ji; Chen, Juxiang; Zhou, Tao; Man, Jianghong; Zhang, Xuemin; Li, Ailing; Pan, Xin

doi:10.1016/j.stem.2022.09.009

Cited by 28 publications

(15 citation statements)

References 57 publications

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“…The aggressiveness of tumor cells is also one of the main malignant phenotypes of glioma, which may be regulated and influenced by the tumor microenvironment [51, 52]. It has been reported that immune checkpoints can affect the expression of MMPs in tumor cells, which promoting the aggressiveness of tumor cells [53, 54].…”

Section: Discussionmentioning

confidence: 99%

Systematic Identification of UBE2C As a Prognostic Biomarker and Correlated with Immunosuppression and Invasiveness in Glioma

Feng,

Fu,

Yang

et al. 2024

Preprint

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Glioma is one of the common tumors of the central nervous system, which presents difficulties in clinical diagnosis and treatment due to its characteristics of immunosuppression and cell invasion phenotypes. If the condition and prognosis of glioma can be predicted during the process of diagnosis and treatment, it will be more conducive to timely intervention or evaluation of glioma. Therefore, we still need to search for more valuable tumor markers. The differential/risk genes and enrichment analysis based on glioma samples (The Cancer Genome Atlas, TCGA). Target gene UBE2C were obtained by the expression correlation and differential expression analysis for the enrichment results. UBE2C were evaluated by clinical grading, survival prognosis and cell experiments. The correlation of UBE2C with immune invasion, immune checkpoint, network analysis and cell invasiveness of gliomas was analyzed by TCGA-glioma data and STRING, respectively. The results suggests that the high expression and risk of UBE2C in gliomas may be a factor that promotes malignant phenotype of tumor cells. The immune phenotype shows that IL6 and IL10 may be the key nodes affecting the immunosuppressive phenotype of glioma. Further, the tumor cells aggressive genes from the MMP family can be correlated with immunosuppressive phenotypes via UBE2C-IL6/IL10 axis, especially displayed by MMP2/MMP9. The UBE2C may systemic effects the malignant phenotype, immunosuppression and cell invasiveness of tumors systematically, which reflects UBE2C as a potential biomarker of glioma and therapeutic target for this tumor.

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Section: Discussionmentioning

confidence: 99%

Systematic Identification of UBE2C As a Prognostic Biomarker and Correlated with Immunosuppression and Invasiveness in Glioma

Feng,

Fu,

Yang

et al. 2024

Preprint

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“…Indeed, Myc binds the histidine decarboxylase (HDC) promoter, which in GSCs is in an open chromatin conformation, bearing a high amount of trimethylated histone H4 on lysine 4 (H3K4me3), as revealed by ATACseq experiments. Released histamine in the extracellular space binds to the histamine H1 receptor on endothelial cells, activating the NF-kB pathway and angiogenesis [ 310 ]. Furthermore, the activation of Myc/HIF1α-dependent aerobic glycolysis gene expression pushes the production of lactate, which is released by GBM cells in the extracellular space, inducing acidosis.…”

Section: Myc and Metabolism In Cancermentioning

confidence: 99%

The “Superoncogene” Myc at the Crossroad between Metabolism and Gene Expression in Glioblastoma Multiforme

Cencioni

Scagnoli

Spallotta

et al. 2023

IJMS

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The concept of the Myc (c-myc, n-myc, l-myc) oncogene as a canonical, DNA-bound transcription factor has consistently changed over the past few years. Indeed, Myc controls gene expression programs at multiple levels: directly binding chromatin and recruiting transcriptional coregulators; modulating the activity of RNA polymerases (RNAPs); and drawing chromatin topology. Therefore, it is evident that Myc deregulation in cancer is a dramatic event. Glioblastoma multiforme (GBM) is the most lethal, still incurable, brain cancer in adults, and it is characterized in most cases by Myc deregulation. Metabolic rewiring typically occurs in cancer cells, and GBM undergoes profound metabolic changes to supply increased energy demand. In nontransformed cells, Myc tightly controls metabolic pathways to maintain cellular homeostasis. Consistently, in Myc-overexpressing cancer cells, including GBM cells, these highly controlled metabolic routes are affected by enhanced Myc activity and show substantial alterations. On the other hand, deregulated cancer metabolism impacts Myc expression and function, placing Myc at the intersection between metabolic pathway activation and gene expression. In this review paper, we summarize the available information on GBM metabolism with a specific focus on the control of the Myc oncogene that, in turn, rules the activation of metabolic signals, ensuring GBM growth.

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“…ECs have also been found to promote GSCs growth and self‐renewal to enhance GBM invasiveness by releasing extracellular vesicles 175 . In turn, brain CSCs can encourage ECs to form blood vessels through multiple mechanisms, providing essential nutrients for the growth of brain tumor 176–179 . Interestingly, brain CSCs can generate blood vessels by transdifferentiation into ECs and pericytes 180–182 …”

Section: Effects Of the Tumor Microenvironment In Brain Tumormentioning

confidence: 99%

Cancer stem cells in brain tumors: From origin to clinical implications

Lin,

Li,

2023

MedComm

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Malignant brain tumors are highly heterogeneous tumors with a poor prognosis and a high morbidity and mortality rate in both children and adults. The cancer stem cell (CSC, also named tumor‐initiating cell) model states that tumor growth is driven by a subset of CSCs. This model explains some of the clinical observations of brain tumors, including the almost unavoidable tumor recurrence after initial successful chemotherapy and/or radiotherapy and treatment resistance. Over the past two decades, strategies for the identification and characterization of brain CSCs have improved significantly, supporting the design of new diagnostic and therapeutic strategies for brain tumors. Relevant studies have unveiled novel characteristics of CSCs in the brain, including their heterogeneity and distinctive immunobiology, which have provided opportunities for new research directions and potential therapeutic approaches. In this review, we summarize the current knowledge of CSCs markers and stemness regulators in brain tumors. We also comprehensively describe the influence of the CSCs niche and tumor microenvironment on brain tumor stemness, including interactions between CSCs and the immune system, and discuss the potential application of CSCs in brain‐based therapies for the treatment of brain tumors.

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Glioblastoma stem cell-specific histamine secretion drives pro-angiogenic tumor microenvironment remodeling

Cited by 28 publications

References 57 publications

Systematic Identification of UBE2C As a Prognostic Biomarker and Correlated with Immunosuppression and Invasiveness in Glioma

Systematic Identification of UBE2C As a Prognostic Biomarker and Correlated with Immunosuppression and Invasiveness in Glioma

The “Superoncogene” Myc at the Crossroad between Metabolism and Gene Expression in Glioblastoma Multiforme

Cancer stem cells in brain tumors: From origin to clinical implications

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