Expression of ecto-5'-nucleotidase (CD73) in normal mammary gland and in breast carcinoma

Krüger, K. H.; Lf, Thompson; Kaufmann, Michael C.; Möller, P.

doi:10.1038/bjc.1991.23

Cited by 35 publications

(27 citation statements)

References 26 publications

(19 reference statements)

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“…One previous study on the expression of eN (CD73) in breast carcinoma did not reveal a significant correlation between eN expression and ER status (56). This could be due to the low number of eN-positive samples (4%) among these tumors.…”

Section: Discussionmentioning

confidence: 76%

Role of Estrogen Receptor in the Regulation of Ecto-5′-Nucleotidase and Adenosine in Breast Cancer

Spychała¹,

Lazarowski²,

Ostapkowicz³

et al. 2004

Clinical Cancer Research

103

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Purpose:The purpose is to understand the expression of ecto-5-nucleotidase (eN), an adenosine producing enzyme with potential roles in angiogenesis, growth, and immunosuppression, in estrogen receptor (ER)-negative and -positive breast cancer.Experimental Design: We investigated the regulation of eN expression at the mRNA and protein levels by ␣ in a panel of breast cancer cell lines that differ in ER status and invasive and metastatic potential. We also determined rates of adenosine formation in cells with high and low eN expression and in ER؉ cells treated with estradiol.Results: ER-negative cells express high eN protein and mRNA levels and produce up to 104-fold more adenosine from AMP and ATP. Estradiol and antiestrogen treatments confirm that eN mRNA and protein expression and adenosine generation are negatively regulated through the ER. Endogenous expression of eN in ER؊ cells transfected with ER␣ and phorbol ester-induced eN expression in ER؉ cells

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Section: Discussionmentioning

confidence: 76%

Role of Estrogen Receptor in the Regulation of Ecto-5′-Nucleotidase and Adenosine in Breast Cancer

Spychała¹,

Lazarowski²,

Ostapkowicz³

et al. 2004

Clinical Cancer Research

103

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“…For the highly invasive human melanoma cell lines, it was shown that CD73 was upregulated and correlated with a number of metastasis-related markers (12). On the contrary, some other clinical research studies showed reduced CD73 activity in breast cancer cells when compared to the adjacent non-involved tissue (21,22). Additionally, the reverse correlation between CD73 activity and metastatic potential was occasionally indicated for rat breast cancer cell lines (35) and B16F10 cells (24,25).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, inhibition of CD73 activity reversed those effects (18,20). Nonetheless, some clinical studies have shown that CD73 exhibits low activity in breast cancer cells when compared to the adjacent non-involved tissue (21,22) and that elevated CD73 expression in tumor cells was a positive prognostic marker for disease-free survival in stage I-III breast cancer patients (23). Therefore, the precise involvement of CD73 in tumor progression requires further clarification.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2013

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Abstract. The role of ecto-5'-nucleotidase (CD73), an enzyme providing interstitial adenosine, was investigated in B16F10 melanoma progression. Chemical inhibition of CD73 decreased adherence of cells to extracellular matrix proteins in vitro and led to enhanced migration and invasion. Both processes were reversed by adenosine receptor agonists. In CD73-deficient mice, tumor growth was decreased in comparison with that of wild-type animals. Additionally, the vasculature of CD73-inhibited tumors was impaired and neoangiogenesis in Matrigel plugs was reduced. It is, therefore, proposed that although CD73 shows anti-invasive and antimigratory function in B16F10 melanoma cells, its proangiogenic action is prevalent in vivo and may contribute to increased tumor growth.

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“…5) inhibit CD8 þ Tcell-mediated immunosurveillance in preclinical models of ovarian cancer. Stromal expression of CD73 has been previously described in the mammary gland (37), but its effect on tumorigenesis was never investigated. Using the ID8 mouse model of ovarian cancer and primary MEF derived from wild-type or CD73-deficient mice as a model of CAFs, we demonstrated that CD73 expression in MEF significantly enhanced ID8 tumorigenesis in vivo and promoted immune escape from CD8 þ T cells.…”

Section: Discussionmentioning

confidence: 99%

CD73 Is Associated with Poor Prognosis in High-Grade Serous Ovarian Cancer

et al. 2015

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The cell surface nucleotidase CD73 is an immunosuppressive enzyme involved in tumor progression and metastasis. Although preclinical studies suggest that CD73 can be targeted for cancer treatment, the clinical impact of CD73 in ovarian cancer remains unclear. In this study, we investigated the prognostic value of CD73 in high-grade serous (HGS) ovarian cancer using gene and protein expression analyses. Our results demonstrate that high levels of CD73 are significantly associated with shorter diseasefree survival and overall survival in patients with HGS ovarian cancer. Furthermore, high levels of CD73 expression in ovarian tumor cells abolished the good prognosis associated with intraepithelial CD8 þ cells. Notably, CD73 gene expression was highest in the C1/stromal molecular subtype of HGS ovarian cancer and positively correlated with an epithelial-to-mesenchymal transition gene signature. Moreover, in vitro studies revealed that CD73 and extracellular adenosine enhance ovarian tumor cell growth as well as expression of antiapoptotic BCL-2 family members. Finally, in vivo coinjection of ID8 mouse ovarian tumor cells with mouse embryonic fibroblasts showed that CD73 expression in fibroblasts promotes tumor immune escape and thereby tumor growth. In conclusion, our study highlights a role for CD73 as a prognostic marker of patient survival and also as a candidate therapeutic target in HGS ovarian cancers.Cancer Res; 75(21); 4494-503. Ó2015 AACR.

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Expression of ecto-5'-nucleotidase (CD73) in normal mammary gland and in breast carcinoma

Cited by 35 publications

References 26 publications

Role of Estrogen Receptor in the Regulation of Ecto-5′-Nucleotidase and Adenosine in Breast Cancer

Role of Estrogen Receptor in the Regulation of Ecto-5′-Nucleotidase and Adenosine in Breast Cancer

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

CD73 Is Associated with Poor Prognosis in High-Grade Serous Ovarian Cancer

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