Ecto-5′-nucleotidase promotes invasion, migration and adhesion of human breast cancer cells

Wang, Li; Zhou, Xing; Zhou, Tingting; Ma, Dong; Chen, SF; Zhi, Xiuling; Li, Yin; Shao, Zhimin; Ou, Zhouluo; Zhou, Ping

doi:10.1007/s00432-007-0292-z

Cited by 166 publications

(142 citation statements)

References 47 publications

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“…Highly expressed in this group of patients with the worst outcome were genes (BMPR1B, CTGF [CCN2], TTYH2, IGJ, PON2, CD73, CDC42EP3, TSPAN7, and SEMA6A) involved in adaptive cell signaling responses to transforming growth factor ␤, stem cell function, B-cell development and differentiation, and the regulation of tumor growth. [27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45] These highest risk cases lacked expression of the genes (NR4A3, BTG3, RGS1, and RGS2) whose relatively high expression characterized the ALL cases with the best outcome. Not surprisingly, given that all cases with an activated kinase signature were assigned to the highest risk group with the combined classifier, 6 of the genes associated with our kinase signature (BMPR1B, ECM1, IGJ, PON2, SEMA6A, and TSPAN7) were contained within our gene expression classifier for RFS.…”

Section: Discussionmentioning

confidence: 99%

Gene expression classifiers for relapse-free survival and minimal residual disease improve risk classification and outcome prediction in pediatric B-precursor acute lymphoblastic leukemia

Kang

Chen

Wilson

et al. 2010

Blood

186

191

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To determine whether gene expression profiling could improve outcome prediction in children with acute lymphoblastic leukemia (ALL) at high risk for relapse, we profiled pretreatment leukemic cells in 207 uniformly treated children with highrisk B-precursor ALL. A 38-gene expression classifier predictive of relapse-free survival (RFS) could distinguish 2 groups with differing relapse risks: low (4-year RFS, 81%, n ‫؍‬ 109) versus high (4-year RFS, 50%, n ‫؍‬ 98; P < .001). In multivariate analysis, the gene expression classifier (P ‫؍‬ .001) and flow cytometric measures of minimal residual disease (MRD; P ‫؍‬ .001) each provided independent prognostic information. Together, they could be used to classify children with high-risk ALL into low-(87% RFS), intermediate-(62% RFS), or high-(29% RFS) risk groups (P < .001). A 21-gene expression classifier predictive of end-induction MRD effectively substituted for flow MRD, yielding a combined classifier that could distinguish these 3 risk groups at diagnosis (P < .001). These classifiers were further validated on an independent highrisk ALL cohort (P ‫؍‬ .006) and retained independent prognostic significance (P < .001) in the presence of other recently described poor prognostic factors (IKAROS/IKZF1 deletions, JAK mutations, and kinase expression signatures

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Section: Discussionmentioning

confidence: 99%

Gene expression classifiers for relapse-free survival and minimal residual disease improve risk classification and outcome prediction in pediatric B-precursor acute lymphoblastic leukemia

Kang

Chen

Wilson

et al. 2010

Blood

186

191

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“…The P1 receptor pathway has also been implicated in promoting cancer cell migration; both CD73 [92,93] and A 2b activity [93] can contribute to this response. Furthermore, adenosine upregulates the expression of the chemokine receptor CXCR4 in cancer cells, an effect that is proposed to occur through the activation of A 2a /A 2b receptors [94].…”

Section: Cancer Cellsmentioning

confidence: 99%

New insights regarding the regulation of chemotaxis by nucleotides, adenosine, and their receptors

Corriden

Insel

2012

Purinergic Signalling

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The directional movement of cells can be regulated by ATP, certain other nucleotides (e.g., ADP, UTP), and adenosine. Such regulation occurs for cells that are "professional phagocytes" (e.g., neutrophils, macrophages, certain lymphocytes, and microglia) and that undergo directional migration and subsequent phagocytosis. Numerous other cell types (e.g., fibroblasts, endothelial cells, neurons, and keratinocytes) also change motility and migration in response to ATP, other nucleotides, and adenosine. In this article, we review how nucleotides and adenosine modulate chemotaxis and motility and highlight the importance of nucleotide-and adenosine-regulated cell migration in several cell types: neutrophils, microglia, endothelial cells, and cancer cells. We also discuss difficulties in conducting experiments and drawing conclusions regarding the ability of nucleotides and adenosine to modulate the migration of professional and non-professional phagocytes.

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“…This enzyme is highly expressed in a variety of solid tumors [19][20][21][22] and has both its enzymatic activity and its adhesion protein function associated with cancer progression [23,24]. Besides, ecto-5′-NT/CD73 was found to be involved in cancer cell growth, maturation, differentiation, adhesion, migration, invasiveness, metastasis, immune escape, and drug resistance [19,[21][22][23][24][25][26][27].…”

Section: Introductionmentioning

confidence: 99%

NTPDase3 and ecto-5′-nucleotidase/CD73 are differentially expressed during mouse bladder cancer progression

Rockenbach

Braganhol

Dietrich

et al. 2014

Purinergic Signalling

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According to the World Health Organization, bladder cancer is the seventh most common cancer among men in the world. The current treatments for this malignancy are not efficient to prevent the recurrence and progression of tumors. Then, researches continue looking for better therapeutic targets which can end up in new and more efficient treatments. One of the recent findings was the identification that the purinergic system was involved in bladder tumorigenesis. The ectonucleotidases, mainly ecto-5′-nucleotidase/CD73 have been revealed as new players in cancer progression and malignity. In this work, we investigated the NTPDase3 and ecto-5′-nucleotidase/CD73 expression in cancer progression in vivo. Bladder tumor was induced in mice by the addition of 0.05 % of N-butyl-N-(hydroxybutyl)-nitrosamine (BBN) in the drinking water for 4, 8, 12, 18, and 24 weeks. After this period, mice bladders were removed for histopathology analysis and immunofluorescence assays. The bladder of animals which has received BBN had alterations, mainly inflammation, in initial times of tumor induction. After 18 weeks, mice's bladder has developed histological alterations similar to human transitional cell carcinoma. The cancerous urothelium, from mice that received BBN for 18 and 24 weeks, presented a weak immunostaining to NTPDase3, in contrast to an increased expression of ecto-5′-nucleotidase/CD73. The altered expression of NTPDase3 and ecto-5′-nucleotidase/ CD73 presented herein adds further evidence to support the idea that alterations in ectonucleotidases are involved in bladder tumorigenesis and reinforce the ecto-5′-nucleotidase/ CD73 as a future biomarker and/or a target for pharmacological therapy of bladder cancer.

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Ecto-5′-nucleotidase promotes invasion, migration and adhesion of human breast cancer cells

Abstract: Taken together, our results indicated that CD73 may facilitate the adhesion, migration and invasion of human breast cancer cells through its enzyme activity of generating adenosine. This study provided a possibly molecular mechanism of metastasis of breast carcinoma.

Cited by 166 publications

References 47 publications

Gene expression classifiers for relapse-free survival and minimal residual disease improve risk classification and outcome prediction in pediatric B-precursor acute lymphoblastic leukemia

Gene expression classifiers for relapse-free survival and minimal residual disease improve risk classification and outcome prediction in pediatric B-precursor acute lymphoblastic leukemia

New insights regarding the regulation of chemotaxis by nucleotides, adenosine, and their receptors

NTPDase3 and ecto-5′-nucleotidase/CD73 are differentially expressed during mouse bladder cancer progression

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