Macrophage/microglia-derived IL-1β induces glioblastoma growth via the STAT3/NF-κB pathway

Kai, Koichi; Komohara, Yoshihiro; Esumi, Shigeyuki; Fujiwara, Yukio; Yamamoto, Takahiro; Uekawa, Ken; Ohta, Kazuhide; Kuroda, Jun-ichiro; Shinojima, Naoki; Hamasaki, Tadashi; Mukasa, Akitake

doi:10.1007/s13577-021-00619-8

Cited by 28 publications

(21 citation statements)

References 32 publications

(34 reference statements)

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“…For the RNA-seq data analysis, the resulting reads were aligned to the human genome (UCSC hg19) using STAR ver.2.6.0a (Dr. Alexander Dobin, Cold Spring Harbor Laboratory, NY, USA) after trimming to remove adapter sequences and low-quality ends using Trim Galore! v0.5.0 (cutadapt v1.16) (Babraham Bioinformatics, Cambridge, UK) [ 29 ]. Gene expression levels were measured in terms of transcripts per million as determined by RSEM v1.3.1 (Dr. Bo Li and Dr. Colin Dewey, University of Wisconsin-Madison, Madison, WI, USA) [ 29 ].…”

Section: Methodsmentioning

confidence: 99%

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SPP1 Derived from Macrophages Is Associated with a Worse Clinical Course and Chemo-Resistance in Lung Adenocarcinoma

Matsubara

Komohara

Esumi

et al. 2022

Cancers

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Osteopontin, also called secreted phosphoprotein 1 (SPP1), is a multifunctional secreted phosphorylated glycoprotein. SPP1 is also expressed in tumor cells, and many studies demonstrated that a high level of circulating SPP1 is correlated with a poor prognosis in various cancers. SPP1 is expressed not only by tumor cells but also by stromal cells, such as macrophages. However, there have been no studies distinguishing the SPP1 expression of cancer cells and tumor-associated macrophages (TAMs). Thus, in this study, we tried to accurately evaluate the SPP1 expression status on cancer cells and TAMs separately in patients with non-small cell lung cancer by using double immunohistochemistry. We demonstrated that high SPP1 expression on TAMs predicted a poor prognosis in lung adenocarcinoma patients. Additionally, we investigated the expression mechanisms related to SPP1 using human-monocyte-derived macrophages and revealed that the SPP1 expression level increased in macrophage differentiation mediated by granulocyte-macrophage colony-stimulating factor. Furthermore, SPP1 contributed to anti-cancer drug resistance in lung cancer cell lines. In conclusion, SPP1 production on TAMs predicted a poor prognosis in lung adenocarcinoma patients, and TAM-derived SPP1′s involvement in the chemo-resistance of cancer cells was suggested.

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Section: Methodsmentioning

confidence: 99%

“…v0.5.0 (cutadapt v1.16) (Babraham Bioinformatics, Cambridge, UK) [ 29 ]. Gene expression levels were measured in terms of transcripts per million as determined by RSEM v1.3.1 (Dr. Bo Li and Dr. Colin Dewey, University of Wisconsin-Madison, Madison, WI, USA) [ 29 ].…”

Section: Methodsmentioning

confidence: 99%

SPP1 Derived from Macrophages Is Associated with a Worse Clinical Course and Chemo-Resistance in Lung Adenocarcinoma

Matsubara

Komohara

Esumi

et al. 2022

Cancers

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“… References: T1: Koo and Duman, 2008 ; T2: Goshen et al, 2008 ; T3: Gajtko et al, 2020 ; T4: Spulber and Schultzberg, 2010 ; T5: Takemiya et al, 2017 ; T6: Clausen et al, 2011 ; T7: Sugama et al, 2011 ; T8: Spulber et al, 2011 ; T9: Liu et al, 2021 ; T10: Liu et al, 2013 ; T11: Viviani et al, 2006 ; T12: Zhu et al, 2006 ; T13: Lai et al, 2006 ; T14: Zhang et al, 2021 ; T15: Tong et al, 2012 ; T16: Patterson, 2015 ; T17: Rage et al, 2006 ; T18: Barrientos et al, 2004 ; T19: Jones et al, 2018 ; T20: Herrera et al, 2019 ; T21: Mai et al, 2019 ; T22: Fleshner et al, 1995 ; T23: Kai et al, 2021 ; T24: Harden et al, 2011 ; T25: Aniszewska et al, 2015 ; T26: Burton et al, 2011 ; T27: Gruol, 2015 ; T28: Sallmann et al, 2000 ; T29: Brown et al, 2014 ; T30: Yang et al, 2017 ; T31: Spooren et al, 2011 ; T32: Streit et al, 2000 ; T33: Schwieler et al, 2015 ; T34: Erta et al, 2012 ; T35: Gruol et al, 2020 ; T36: Hernandez et al, 2016 ; T37: Strle et al, 2001 ; T38: Perez-Asensio et al, 2013 ; T39: Sawada et al, 1999 ; T40: Laffer et al, 2019 ; T41: Balasingam and Yong, 1996 ; T42: Kvaratskhelia et al, 2009 ; T43: Zhou et al, 2009 ; T44: Burmeister and Marriott, 2018 ; T45: Lobo-Silva et al, 2016 ; T46: Kelly et al, 2001 ; T47: Nenov et al, 2019 ; T48: Ledeboer et al, 2000 ; T49: Molina-H...…”

Section: Cytokines and Kynureninesunclassified

An integrated cytokine and kynurenine network as the basis of neuroimmune communication

et al. 2022

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Two of the molecular families closely associated with mediating communication between the brain and immune system are cytokines and the kynurenine metabolites of tryptophan. Both groups regulate neuron and glial activity in the central nervous system (CNS) and leukocyte function in the immune system, although neither group alone completely explains neuroimmune function, disease occurrence or severity. This essay suggests that the two families perform complementary functions generating an integrated network. The kynurenine pathway determines overall neuronal excitability and plasticity by modulating glutamate receptors and GPR35 activity across the CNS, and regulates general features of immune cell status, surveillance and tolerance which often involves the Aryl Hydrocarbon Receptor (AHR). Equally, cytokines and chemokines define and regulate specific populations of neurons, glia or immune system leukocytes, generating more specific responses within restricted CNS regions or leukocyte populations. In addition, as there is a much larger variety of these compounds, their homing properties enable the superimposition of dynamic variations of cell activity upon local, spatially limited, cell populations. This would in principle allow the targeting of potential treatments to restricted regions of the CNS. The proposed synergistic interface of ‘tonic’ kynurenine pathway affecting baseline activity and the superimposed ‘phasic’ cytokine system would constitute an integrated network explaining some features of neuroimmune communication. The concept would broaden the scope for the development of new treatments for disorders involving both the CNS and immune systems, with safer and more effective agents targeted to specific CNS regions.

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“…Despite the growing body of evidence on the topic reported in this paper, many aspects are yet to be explored in the field [ 4 , 26 , 45 , 54 , 98 , 101 , 102 ]. The correct and extensive understanding of microglia–glioma crosstalk could help in understanding the physiopathology of this complex disease, possibly opening scenarios for improvement of surgical strategies and medical treatments.…”

Section: Discussionmentioning

confidence: 99%

Glioma-Associated Microglia Characterization in the Glioblastoma Microenvironment through a ‘Seed-and Soil’ Approach: A Systematic Review

et al. 2022

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Ever since the discovery of tumor-associated immune cells, there has been growing interest in the understanding of the mechanisms underlying the crosstalk between these cells and tumor cells. A “seed and soil” approach has been recently introduced to describe the glioblastoma (GBM) landscape: tumor microenvironments act as fertile “soil” and interact with the “seed” (glial and stem cells compartment). In the following article, we provide a systematic review of the current evidence pertaining to the characterization of glioma-associated macrophages and microglia (GAMs) and microglia and macrophage cells in the glioma tumor microenvironment (TME). Methods: An online literature search was launched on PubMed Medline and Scopus using the following research string: “((Glioma associated macrophages OR GAM OR Microglia) AND (glioblastoma tumor microenvironment OR TME))”. The last search for articles pertinent to the topic was conducted in February 2022. Results: The search of the literature yielded a total of 349 results. A total of 235 studies were found to be relevant to our research question and were assessed for eligibility. Upon a full-text review, 58 articles were included in the review. The reviewed papers were further divided into three categories based on their focus: (1) Microglia maintenance of immunological homeostasis and protection against autoimmunity; (2) Microglia crosstalk with dedifferentiated and stem-like glioblastoma cells; (3) Microglia migratory behavior and its activation pattern. Conclusions: Aggressive growth, inevitable recurrence, and scarce response to immunotherapies are driving the necessity to focus on the GBM TME from a different perspective to possibly disentangle its role as a fertile ‘soil’ for tumor progression and identify within it feasible therapeutic targets. Against this background, our systematic review confirmed microglia to play a paramount role in promoting GBM progression and relapse after treatments. The correct and extensive understanding of microglia–glioma crosstalk could help in understanding the physiopathology of this complex disease, possibly opening scenarios for improvement of treatments.

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Macrophage/microglia-derived IL-1β induces glioblastoma growth via the STAT3/NF-κB pathway

Cited by 28 publications

References 32 publications

SPP1 Derived from Macrophages Is Associated with a Worse Clinical Course and Chemo-Resistance in Lung Adenocarcinoma

SPP1 Derived from Macrophages Is Associated with a Worse Clinical Course and Chemo-Resistance in Lung Adenocarcinoma

An integrated cytokine and kynurenine network as the basis of neuroimmune communication

Glioma-Associated Microglia Characterization in the Glioblastoma Microenvironment through a ‘Seed-and Soil’ Approach: A Systematic Review

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