Ecto-5′-Nucleotidase (eN, CD73) is Coexpressed with Metastasis Promoting Antigens in Human Melanoma Cells

Sądej, Rafał; Spychała, Józef; Składanowski, Andrzej C.

doi:10.1080/15257770600894188

Cited by 36 publications

(31 citation statements)

References 7 publications

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“…Previous studies have revealed that CD73 is applicable as a cell-surface marker of malignant tumors, including those in bladder cancer (22), leukemia (23), glioma (24), melanoma (25), and ovarian (26), colon, breast (7,24,(27)(28)(29), thyroid (30), esophageal (31) and prostate cancers (32). However, to the best of our knowledge, the present study is the first to report that CD73 may also be a biomarker for clear cell RCC.…”

contrasting

confidence: 41%

Ecto-5′-nucleotidase expression is associated with the progression of renal cell carcinoma

Wang

Song

et al. 2015

Oncology Letters

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Abstract. Renal cell carcinoma (RCC) is a common tissue tumor that occurs across all age groups and has become one of the types of cancer with the fastest increasing incidence. Due to the resistance of RCC chemo-and radiotherapy, surgery is the only currently effective treatment. Therefore, specific markers for the diagnosis and prognosis of RCC are expected to result in novel methods of treatment. Ecto-5'-nucleotidase, also termed cluster of differentiation (CD)73, is a protein that is activated in several types of aggressive cancer and may promote cancer progression. CD73 was examined in the present study to determine the association between the protein and RCC. The expression levels of CD73 in 159 RCC tissue sections and 30 paratumorous normal renal tissue samples obtained from 235 patients that underwent nephrectomy were examined by immunohistochemical staining. By contrast, the expression level of P-glycoprotein (P-gp), a potential prognostic factor in RCC, was also examined in 85 RCC and 13 normal tissue samples. Intense CD73 expression was identified in 75 out of 159 RCC cell membranes compared with normal renal tissues. In contrast, there was high P-gp expression in the blood vessels of 42 out of 85 RCC tissues and there was no significant difference between the P-gp expression identified in RCC cells (34 out of 85) and the cell membrane of normal renal cells (2 out of 13). The expression level of CD73 in RCC cells was significantly associated with tumor type, tumor node metastasis (TNM) stage, and tumor grade. However, the expression of P-gp in RCC cells was only associated with the TNM stage and tumor grade. Using a multivariable Cox regression analysis, it was found that the median survival rate of RCC patients with intense CD73 expression in RCC cells was 62.06±5.35 months, which was drastically shorter compared with rare CD73 expression (103.72±3.67 months). In conclusion, the expression level of CD73 is significantly associated with RCC tumor progression and may serve as a favorable marker for the diagnosis and prognosis of RCC, in addition to being a therapeutic target for the treatment of RCC.

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contrasting

confidence: 41%

Ecto-5′-nucleotidase expression is associated with the progression of renal cell carcinoma

Wang

Song

et al. 2015

Oncology Letters

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“…Department of Medicine; Cancer Therapy & Research Center; University of Texas Health Sciences Center; San Antonio, TX USA Previous studies reported that CD73 participates in cell-cell and cell-matrix interactions 7,8 and implicated CD73 in drug resistance 9 and tumor-promotion.…”

Section: Bin Zhangmentioning

confidence: 99%

“…In addition to the immunoregulatory roles of CD73, the participation of CD73 per se as a proliferative factor, being involved in the control of cell growth, differentiation, invasion, migration and metastasis processes has been established. 10,11 Moreover, CD73-derived adenosine can directly enhance tumor cell adhesion 7,8 and/or chemotaxis. 19 It is also intriguing that CD73 may contribute to tumor angiogenesis.…”

Section: Implications and Future Directionsmentioning

confidence: 99%

CD73 promotes tumor growth and metastasis

Zhang¹

2012

OncoImmunology

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“…CD73 expression on tumor cells has been reported in several types of cancer, including bladder cancer (19), leukemia (20), glioma (21), glioblastoma (22), melanoma (23), ovarian cancer (24), thyroid cancer (25), esophageal cancer (26), prostate cancer (27), and breast cancer (28,29). Notably, CD73 expression has been associated with a prometastatic phenotype in melanoma and breast cancer (23,30,31).…”

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confidence: 99%

Anti-CD73 antibody therapy inhibits breast tumor growth and metastasis

Stagg

Divisekera

McLaughlin

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

503

534

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Extracellular adenosine is a potent immunosuppressor that accumulates during tumor growth. We performed proof-of-concept studies investigating the therapeutic potential and mechanism of action of monoclonal antibody (mAb)-based therapy against CD73, an ecto-enzyme overexpressed on breast-cancer cells that catalyzes the dephosphorylation of adenosine monophosphates into adenosine. We showed that anti-CD73 mAb therapy significantly delayed primary 4T1.2 and E0771 tumor growth in immune-competent mice and significantly inhibited the development of spontaneous 4T1.2 lung metastases. Notably, anti-CD73 mAb therapy was essentially dependent on the induction of adaptive anti-tumor immune responses. Knockdown of CD73 in 4T1.2 tumor cells confirmed the tumor-promoting effects of CD73. In addition to its immunosuppressive effect, CD73 enhanced tumor-cell chemotaxis, suggesting a role for CD73-derived adenosine in tumor metastasis. Accordingly, administration of adenosine-5′-N-ethylcarboxamide to tumorbearing mice significantly enhanced spontaneous 4T1.2 lung metastasis. Using selective adenosine-receptor antagonists, we showed that activation of A2B adenosine receptors promoted 4T1.2 tumorcell chemotaxis in vitro and metastasis in vivo. In conclusion, our study identified tumor-derived CD73 as a mechanism of tumor immune escape and tumor metastasis, and it also established the proof of concept that targeted therapy against CD73 can trigger adaptive anti-tumor immunity and inhibit metastasis of breast cancer.adenosine | cancer | chemotaxis | immunosuppression | regulatory

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Ecto-5′-Nucleotidase (eN, CD73) is Coexpressed with Metastasis Promoting Antigens in Human Melanoma Cells

Cited by 36 publications

References 7 publications

Ecto-5′-nucleotidase expression is associated with the progression of renal cell carcinoma

Ecto-5′-nucleotidase expression is associated with the progression of renal cell carcinoma

CD73 promotes tumor growth and metastasis

Anti-CD73 antibody therapy inhibits breast tumor growth and metastasis

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