CD73 is associated with poor prognosis in HNSCC

Ren, Zhenhu; Lin, Chengzhong; Cao, Wei; Yang, Rong; Lü, Wei; Liu, Zheqi; Chen, Yiming; Yang, Xi; Tian, Zhen; Wang, Lizhen; Jiang, Li; Xu, Wei; Chen, Wantao; Ji, Tong; Zhang, Chenping

doi:10.18632/oncotarget.11435

Cited by 59 publications

(48 citation statements)

References 43 publications

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“…Conversely, it has also been reported that inosine-mediated activation of the A3R can enhance melanoma cell proliferation through activation of the ERK pathway [100] and a cytoprotective role for the A3R has also been described [101]. Similarly, activation of the A3R has been suggested to enhance the migration or invasion of tumor cells [73,102,103]. Notably, in one study, divergent effects of A3R activation (via IB-MECA stimulation) on proliferation were observed in two colorectal cancer lines.…”

Section: Expression Of Adenosine Receptors and Signaling Pathways In mentioning

confidence: 95%

Targeting Adenosine Receptor Signaling in Cancer Immunotherapy

Sek¹,

Mølck²,

Stewart³

et al. 2018

Preprint

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The immune system plays a major role in the surveillance and control of malignant cells, with the presence of tumor infiltrating lymphocytes (TILs) correlating with better patient prognosis in multiple tumor types. The development of ‘checkpoint blockade’ and adoptive cellular therapy has revolutionized the landscape of cancer treatment and highlights the potential of utilizing the patient’s own immune system to eradicate cancer. One mechanism of tumor-mediated immunosuppression that has gained attention as a potential therapeutic target is the purinergic signaling axis, whereby the production of the purine nucleoside adenosine in the tumor microenvironment can potently suppress T and NK cell function. The production of extracellular adenosine is mediated by the cell surface ectoenzymes CD73, CD39 and CD38 and therapeutic agents have been developed to target these as well as the downstream adenosine receptors (A1R, A2AR, A2BR, A3R) to enhance anti-tumor immune responses. This review will discuss the role of adenosine and adenosine receptor signaling in tumor and immune cells with a focus on their cell-specific function and their potential as targets in cancer immunotherapy.

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Section: Expression Of Adenosine Receptors and Signaling Pathways In mentioning

confidence: 95%

Targeting Adenosine Receptor Signaling in Cancer Immunotherapy

Sek¹,

Mølck²,

Stewart³

et al. 2018

Preprint

View full text Add to dashboard Cite

show abstract

“…CD73-deficient mice were demonstrated to sustain activated antitumor immunity, influencing neovascularization, tumor growth and metastasis [119,120]. CD73 inactivation was proved to inhibit progression of breast cancer and head and neck squamous cell carcinoma [121,122]. Likewise, anti-CD73 blocking antibody was also documented to impact spontaneous lung metastasis and decrease circulation capability of cancer cells [4].…”

Section: Cd39 and Cd73 As Tumor Therapeutic Targetsmentioning

confidence: 99%

The yin and yang functions of extracellular ATP and adenosine in tumor immunity

Cai

Zhu

et al. 2020

Cancer Cell Int

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Extracellular adenosine triphosphate (eATP) and its main metabolite adenosine (ADO) constitute an intrinsic part of immunological network in tumor immunity. The concentrations of eATP and ADO in tumor microenvironment (TME) are controlled by ectonucleotidases, such as CD39 and CD73, the major ecto-enzymes expressed on immune cells, endothelial cells and cancer cells. Once accumulated in TME, eATP boosts antitumor immune responses, while ADO attenuates immunity against tumors. eATP and ADO, like yin and yang, represent two opposite aspects from immuneactivating to immune-suppressive signals. Here we reviewed the functions of eATP and ADO in tumor immunity and attempt to block eATP hydrolysis, ADO formation and their contradictory effects in tumor models, allowing the induction of effective anti-tumor immune responses in TME. These attempts documented that therapeutic approaches targeting eATP/ADO metabolism and function may be effective methods in cancer therapy.

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“…1 Ecto-5 0 -nucleotidase (CD73), a 70 kDa glycosylated protein bounding to the outer surface of the plasma membrane by a glycosyl phosphatidyl inositol (GPI) anchor, is over-expressed in a variety of tumors, including breast cancer. [2][3][4][5] Major function of CD73 is catalyzing extracellular 5 0 -AMP to adenosine that plays important roles in many physiological and pathophysiological circumstances through adenosine receptor (A1, A2A, A2B and A3 AR). 6 Up-regulation of CD73 is associated with highly invasive cancer phenotype, drug resistance and tumor-promoting functions.…”

mentioning

confidence: 99%

Extracellular 5′‐nucleotidase (CD73) promotes human breast cancer cells growth through AKT/GSK‐3β/β‐catenin/cyclinD1 signaling pathway

Wang

Lü

et al. 2017

Intl Journal of Cancer

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To identify the role and to explore the mechanism of extracellular 5'-nucleotidase (CD73) in human breast cancer growth, CD73 expression was measured firstly in breast cancer tissues and cell lines, and then interfered with or over-expressed by recombinant lentivirus in cell lines. Impacts of CD73 on breast cancer cell proliferation and cell cycle were investigated with colony formation assay, CCK-8 and flow cytometry. The relationship between CD73 and AKT/GSK-3β/β-catenin pathway was assessed with adenosine, adenosine 2A receptor antagonist (SCH-58261), adenosine 2A receptor agonist (NECA), CD73 enzyme inhibitor (APCP) and Akt inhibitor (MK-2206). Moreover, the effect of CD73 on breast cancer growth in vivo was examined with human breast cancer transplanting model of nude mice. The results showed that the expression of CD73 was high in breast cancer tissues and increased with advanced tumor grades and lympho-node status. CD73 expression was higher in more malignant cells, and CD73 overexpression promoted breast cancer cell proliferation in both in vivo and in vitro. It activated AKT/GSK-3β/β-catenin/cyclinD1 signaling pathway through CD73 enzyme activity and other mechanism.

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CD73 is associated with poor prognosis in HNSCC

Cited by 59 publications

References 43 publications

Targeting Adenosine Receptor Signaling in Cancer Immunotherapy

Targeting Adenosine Receptor Signaling in Cancer Immunotherapy

The yin and yang functions of extracellular ATP and adenosine in tumor immunity

Extracellular 5′‐nucleotidase (CD73) promotes human breast cancer cells growth through AKT/GSK‐3β/β‐catenin/cyclinD1 signaling pathway

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