Current advances in modulating tumor hypoxia for enhanced therapeutic efficacy

Liu, Zihan; Liu, Xinping; Zhang, Wei; Gao, Ruijie; Wei, Hua; Yu, Cui-Yun

doi:10.1016/j.actbio.2024.01.010

Cited by 3 publications

(1 citation statement)

References 265 publications

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“…Hypoxia creates an abnormal TME in which angiogenesis is constantly upregulated and immune system functions are limited (e.g., recruitment of tumor-infiltrating lymphocytes -TILs), which lead to tumor-mediated immunosuppression [315]. Hypoxia contributes to the progression of cancer and resistance to photodynamic therapy, chemotherapy and radiotherapy [316][317][318].…”

Section: Hypoxia and Angiogenesis In The Tumor Microenvironment (Tme)mentioning

confidence: 99%

CX3CL1 (Fractalkine)-CX3CR1 Axis in Inflammation-Induced Angiogenesis and Tumorigenesis

Szukiewicz

2024

Preprint

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The chemotactic cytokine fractalkine (FKN, chemokine CX3CL1) has unique properties resulting from the combination of chemoattractants and adhesion molecules. The soluble form (sFKN) has chemotactic properties and potently attracts T cells and monocytes. The membrane-bound form (mFKN) facilitates diapedesis and is responsible for cell-to-cell adhesion, especially by promoting the strong adhesion of leukocytes (monocytes) to activated endothelial cells with the subsequent formation of an extracellular matrix and angiogenesis. FKN signaling occurs via CX3CR1, which is the only known member of the CX3C chemokine receptor subfamily. Signaling within the FKN-CX3CR1 axis plays an important role in many processes related to inflammation and the immune response, which often occur simultaneously and overlap. FKN is strongly upregulated by hypoxia and/or inflammation-induced inflammatory cytokine secretion, and it may act locally as a key angiogenic factor in the highly hypoxic tumor microenvironment. The importance of the FKN/CX3CR1 signaling pathway in tumorigenesis and cancer metastasis results from its influence on cell adhesion, apoptosis and cell migration. This review presents the role of the FKN signaling pathway in the context of angiogenesis in inflammation and cancer. The mechanisms determining the pro- or anti-tumor effects are presented, which are the cause of the seemingly contradictory results that create confusion regarding the therapeutic goals.

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Section: Hypoxia and Angiogenesis In The Tumor Microenvironment (Tme)mentioning

confidence: 99%

CX3CL1 (Fractalkine)-CX3CR1 Axis in Inflammation-Induced Angiogenesis and Tumorigenesis

Szukiewicz

2024

Preprint

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Natural-product-based, carrier-free, noncovalent nanoparticles for tumor chemo-photodynamic combination therapy

Wang,

Yang

2024

Pharmacological Research

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CX3CL1 (Fractalkine)-CX3CR1 Axis in Inflammation-Induced Angiogenesis and Tumorigenesis

Szukiewicz

2024

IJMS

View full text Add to dashboard Cite

The chemotactic cytokine fractalkine (FKN, chemokine CX3CL1) has unique properties resulting from the combination of chemoattractants and adhesion molecules. The soluble form (sFKN) has chemotactic properties and strongly attracts T cells and monocytes. The membrane-bound form (mFKN) facilitates diapedesis and is responsible for cell-to-cell adhesion, especially by promoting the strong adhesion of leukocytes (monocytes) to activated endothelial cells with the subsequent formation of an extracellular matrix and angiogenesis. FKN signaling occurs via CX3CR1, which is the only known member of the CX3C chemokine receptor subfamily. Signaling within the FKN-CX3CR1 axis plays an important role in many processes related to inflammation and the immune response, which often occur simultaneously and overlap. FKN is strongly upregulated by hypoxia and/or inflammation-induced inflammatory cytokine release, and it may act locally as a key angiogenic factor in the highly hypoxic tumor microenvironment. The importance of the FKN/CX3CR1 signaling pathway in tumorigenesis and cancer metastasis results from its influence on cell adhesion, apoptosis, and cell migration. This review presents the role of the FKN signaling pathway in the context of angiogenesis in inflammation and cancer. The mechanisms determining the pro- or anti-tumor effects are presented, which are the cause of the seemingly contradictory results that create confusion regarding the therapeutic goals.

show abstract

Current advances in modulating tumor hypoxia for enhanced therapeutic efficacy

Cited by 3 publications

References 265 publications

CX3CL1 (Fractalkine)-CX3CR1 Axis in Inflammation-Induced Angiogenesis and Tumorigenesis

CX3CL1 (Fractalkine)-CX3CR1 Axis in Inflammation-Induced Angiogenesis and Tumorigenesis

Natural-product-based, carrier-free, noncovalent nanoparticles for tumor chemo-photodynamic combination therapy

CX3CL1 (Fractalkine)-CX3CR1 Axis in Inflammation-Induced Angiogenesis and Tumorigenesis

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