RETRACTED ARTICLE: SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway

Han, Shuai; Wei, Zhen; Guo, Tongqi; Zou, Jianjun; Li, Fuyong

doi:10.1186/s13046-020-01730-8

Cited by 15 publications

(9 citation statements)

References 54 publications

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“…SET domain bifurcated 1 (SETDB1) is upregulated in GBM and promotes AKT/mTOR-dependent CSF-1 induction and secretion, which leads to macrophage recruitment in the tumor, resulting in tumor growth. Thus it is relative to poor progression [30].…”

Section: Gbm On Gamsmentioning

confidence: 99%

Macrophages/Microglia in the Glioblastoma Tumor Microenvironment

Chen

2021

IJMS

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The complex interaction between glioblastoma and its microenvironment has been recognized for decades. Among various immune profiles, the major population is tumor-associated macrophage, with microglia as its localized homolog. The present definition of such myeloid cells is based on a series of cell markers. These good sentinel cells experience significant changes, facilitating glioblastoma development and protecting it from therapeutic treatments. Huge, complicated mechanisms are involved during the overall processes. A lot of effort has been dedicated to crack the mysterious codes in macrophage/microglia recruiting, activating, reprogramming, and functioning. We have made our path. With more and more key factors identified, a lot of new therapeutic methods could be explored to break the ominous loop, to enhance tumor sensitivity to treatments, and to improve the prognosis of glioblastoma patients. However, it might be a synergistic system rather than a series of clear, stepwise events. There are still significant challenges before the light of truth can shine onto the field. Here, we summarize recent advances in this field, reviewing the path we have been on and where we are now.

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Section: Gbm On Gamsmentioning

confidence: 99%

Macrophages/Microglia in the Glioblastoma Tumor Microenvironment

Chen

2021

IJMS

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“…CSF1R, a type III protein tyrosine kinase receptor, is widely expressed by TAMs ( 70 ). The activation of CSF1R signaling by IL-34 or CSF1 induces the recruitment of macrophages and shifts the TAM phenotype from M1 to M2 ( 71 – 73 ). Pexidartinib (PLX3397), the first commercial CSF1R inhibitor approved by the Food and Drug Administration (FDA), was recently used in a phase II clinical trial of recurrent glioblastoma (NCT01349036).…”

Section: Tam-targeting Therapies For Gbmmentioning

confidence: 99%

Targeting tumor-associated macrophages for the immunotherapy of glioblastoma: Navigating the clinical and translational landscape

et al. 2022

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Tumor-associated macrophages (TAMs) can directly clear tumor cells and enhance the phagocytic ability of immune cells. An abundance of TAMs at the site of the glioblastoma tumor indicates that TAM-targeting immunotherapy could represent a potential form of treatment for this aggressive cancer. Herein, we discuss: i) the dynamic role of TAMs in glioblastoma; ii) describe the formation of the immunosuppressive tumor microenvironment; iii) summarize the latest clinical trial data that reveal how TAM function can be regulated in favor tumor eradication; and lastly, iv) evaluate the implications of existing and novel translational approaches for treating glioblastoma in clinical practice.

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“…Han et al. demonstrated that SETDB1 promoted AKT/mTOR-dependent CSF-1 induction and secretion, leading to macrophage recruitment in the tumor, and subsequently contributing to tumor growth ( 67 ). Additionally, De Boeck et al.…”

Section: Effects Of Glioblastoma On Tamsmentioning

confidence: 99%

Signal Pathways Involved in the Interaction Between Tumor-Associated Macrophages/TAMs and Glioblastoma Cells

Liu

et al. 2022

Front. Oncol.

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It is commonly recognized, that glioblastoma is a large complex composed of neoplastic and non-neoplastic cells. Tumor-associated macrophages account for the majority of tumor bulk and play pivotal roles in tumor proliferation, migration, invasion, and survival. There are sophisticated interactions between malignant cells and tumor associated-macrophages. Tumor cells release a variety of chemokines, cytokines, and growth factors that subsequently lead to the recruitment of TAMs, which in return released a plethora of factors to construct an immunosuppressive and tumor-supportive microenvironment. In this article, we have reviewed the biological characteristics of glioblastoma-associated macrophages and microglia, highlighting the emerging molecular targets and related signal pathways involved in the interaction between TAMs and glioblastoma cells, as well as the potential TAMs-associated therapeutic targets for glioblastoma.

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RETRACTED ARTICLE: SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway

Cited by 15 publications

References 54 publications

Macrophages/Microglia in the Glioblastoma Tumor Microenvironment

Macrophages/Microglia in the Glioblastoma Tumor Microenvironment

Targeting tumor-associated macrophages for the immunotherapy of glioblastoma: Navigating the clinical and translational landscape

Signal Pathways Involved in the Interaction Between Tumor-Associated Macrophages/TAMs and Glioblastoma Cells

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