Inhibition of CD73 stimulates the migration and invasion of B16F10 melanoma cells in vitro, but results in impaired angiogenesis and reduced melanoma growth in vivo

Koszałka, Patrycja; Pryszlak, Anna; Gołuńska, Monika; Kolasa, Justyna; Stasiłojć, Grzegorz; Składanowski, Andrzej C.; Bigda, Jacek

doi:10.3892/or.2013.2883

Cited by 31 publications

(22 citation statements)

References 40 publications

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“…In meduloblastoma cell lines, the metastatic potential is inversely correlated with CD73 expression and activity [35]. Pharmacological inhibition of CD73 reduces adhesion but increases the invasion/migration capacities in vitro [17, 36], and treatment with adenosine (produced by CD73) inhibits cell migration and invasion [37]. More recently, loss of CD73 has been involved in epithelial barrier misstructuration and endometrial tumor progression [17].…”

Section: Discussionmentioning

confidence: 99%

MiR-422a promotes loco-regional recurrence by targeting NT5E/CD73 in head and neck squamous cell carcinoma

et al. 2016

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At the time of diagnosis, 60% of patients with head and neck squamous cell carcinoma (HNSCC) present tumors in an advanced stage (III-IV) of disease and 80% will relapse within the first two years post-treatment, due to their frequent radio(chemo)resistance. To identify new molecular targets and companion biomarkers, we have investigated the miRNome of 75 stage III-IV oropharynx tumors without relapse (R) or with loco-regional relapse (non-responder, NR) within two years post-treatment. Interestingly, miR-422a was significantly downregulated in NR tumors, in agreement with the increase in cell proliferation and adhesion induced by miR-422a inhibition in vitro. Furthermore, we identified CD73/NT5E oncogene as target of miR-422a. Indeed, modulation of the endogenous level of miR-422a inversely influences the expression and the enzymatic activity of CD73. Moreover, knocking down CD73 mimics the effects of miR-422a upregulation. Importantly, in tumors, miR-422a and CD73 expression levels are inversely correlated, and both are predictive of relapse free survival - especially considering loco(regional) recurrence - in vitro two independent cohorts of advanced oropharynx or HNSCC (N=255) tumors. In all, we reported, for the first time, that MiR-422a and its target CD73 are involved in early loco(regional) recurrence of HNSCC tumors and are new targets for personalized medicine.

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Section: Discussionmentioning

confidence: 99%

MiR-422a promotes loco-regional recurrence by targeting NT5E/CD73 in head and neck squamous cell carcinoma

et al. 2016

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“…A role for CD73 in supporting tumor angiogenesis was established both in vitro and in vivo [11, 18, 86, 87]. CD73 promotes the formation of new vessels in C57BL/6 mice bearing B16F10 melanoma cells and tumor-induced angiogenesis in Matrigel plugs [18].…”

Section: Regulation Of Cancer Immunity By Cd73mentioning

confidence: 99%

“…CD73 promotes the formation of new vessels in C57BL/6 mice bearing B16F10 melanoma cells and tumor-induced angiogenesis in Matrigel plugs [18]. The pharmacological inhibition of CD73 decreases the development of melanoma vascular beds by reducing the number or the maturation of developing new blood vessels[18]. CD73 can also promote microvascular endothelial cell migration and the formation of tube-like structures[86].…”

Section: Regulation Of Cancer Immunity By Cd73mentioning

confidence: 99%

Anti-CD73 in Cancer Immunotherapy: Awakening New Opportunities

et al. 2016

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In recent years, cancer immunotherapy made significant advances due to a better understanding of the principles underlying tumor biology and immunology. In this context, CD73 is a key molecule, since via degradation of adenosine monophosphate into adenosine, endorses the generation of an immunosuppressed and pro-angiogenic niche within the tumor microenvironment that promotes the onset and progression of cancer. Targeting CD73 results in favorable antitumor effects in pre-clinical models and combined treatments of CD73 blockade with other immune-modulating agents (i.e. anti-CTLA-4 mAb or anti-PD1 mAb) is particularly attractive. Although there is still a long way to go, anti-CD73 therapy, through the development of CD73 monoclonal antibodies, can potentially constitute a new biologic therapy for cancer patients. In this review, we discuss the link between CD73 and the onset, development and spread of tumors, highlighting the potential value of this molecule as a target and as a novel biomarker in the context of personalized cancer therapy

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“…Recently, Koszalka et al reported that inhibition of CD73 resulted in impaired angiogenesis and reduced melanoma growth in mice models [44]. Allard et al investigated the importance of CD73 expression during tumor angiogenesis and the effect of anti-CD73 mAb therapy on angiogenesis.…”

Section: Cd73 and Tumor Angiogenesismentioning

confidence: 99%

The Roles of CD73 in Cancer

Gao

Dong

Zhang

2014

BioMed Research International

165

141

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Purinergic signaling has emerged as an important player in cancer progression and is regulated by a series of nucleotidases. Among the enzyme cascade, CD73, which catelyzes AMP breakdown to adenosine, has been found to be overexpressed in many types of cancer. Various factors and mechanisms are employed to regulate expression of CD73. Accumulating studies have shown that CD73 is a key regulatory molecule of cancer cells proliferation, migration and invasion in vitro, tumor angiogenesis, and tumor immune escape in vivo. With such important roles in cancer, CD73 has become an appealing therapy target. Recent evidences in mice models demonstrated that targeted blockade of CD73 could be a favorable therapeutic approach for cancer patients in the future. In this review, we will summarize the multiple roles of CD73 in cancer development, including its clinical significance, its promotive effects on tumor growth, metastasis, and angiogenesis, and its suppressive effects on immune response, regulatory mechanisms of CD73 expression, and current situation of anti-CD73 cancer therapy.

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Inhibition of CD73 stimulates the migration and invasion of B16F10 melanoma cells in vitro, but results in impaired angiogenesis and reduced melanoma growth in vivo

Cited by 31 publications

References 40 publications

MiR-422a promotes loco-regional recurrence by targeting NT5E/CD73 in head and neck squamous cell carcinoma

MiR-422a promotes loco-regional recurrence by targeting NT5E/CD73 in head and neck squamous cell carcinoma

Anti-CD73 in Cancer Immunotherapy: Awakening New Opportunities

The Roles of CD73 in Cancer

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