NDPKA is not just a metastasis suppressor – be aware of its metastasis-promoting role in neuroblastoma

Tan, Choon-Yee; ␣Chang, Christina L.

doi:10.1038/labinvest.2017.105

Cited by 23 publications

(22 citation statements)

References 155 publications

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“…The nucleoside kinases of NME1, NME2P1, UCK2 and UCK1, within in these terms, were significantly upregulated as USP7 downregulation, indicating that USP7 impacted on the nucleotides-metabolism-associated protome. Additionally, one of these, NME1, was reported as a metastasis suppressor according previous studies 34 , which provided a clue to explain how USP7 influence on metastasis of melanoma.…”

Section: Bioinformatics Analysismentioning

confidence: 83%

USP7 regulates melanoma progression through PI3K/Akt/FOXO and AMPK Pathways

Teichmann

Jia

Gao

et al. 2020

Preprint

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Background: Increasing evidence suggests that deubiquitinase USP7 participates in tumor progression by various mechanisms and serves as a potential therapeutic target. However, its functional role in melanoma remains elusive and needs to be investigated. Methods: The down-regulation of USP7 in A375 human melanoma cells was determined by high resolution liquid chromatography mass spectrometry (LC-MS/MS). The effects of USP7 expression on proliferation and apoptosis of melanoma cells were examined by western blot, Immunohistochemical and flow cytometry. Further study knock-down of USP7 in A375 cell lines, especially knockout USP7 using CRISPR-Cas9, verified USP7 regulate cell proliferation in vivo and in vitro .Western blot and qRT-PCR, Immunofluorescence were performed to investigate the mechanisms by which USP7 mediated melanoma growth through regulating the PI3K/Akt/FOXO pathways activity Results: Proteomic and western blotting analysis show that inhibition of USP7 increases expression of PRKAB1, CASP7, and PPP2R3A, attenuates expression of ATP6V0C and PEX11B. Furthermore, ATP6V0C and PEX11B are proposed to be the substrate for USP7 function. Conclusions: Our findings demonstrate that PI3K/Akt/FOXO and AMPK signaling pathways can be regulated by USP7 during melanoma progression and provide USP7 as an attractive anticancer target for melanoma.

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Section: Bioinformatics Analysismentioning

confidence: 83%

USP7 regulates melanoma progression through PI3K/Akt/FOXO and AMPK Pathways

Teichmann

Jia

Gao

et al. 2020

Preprint

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“…Studies in neuroblastoma also reported a positive correlation between NM23-H1 expression and tumor progression [24,25]. Moreover, in aggressive cases a S120G missense mutation was identified, which seems to be specific for this tumor type [24,26]. It is important to note that NM23-H1 as a representing MSG is very rarely mutated in different tumor types, unlike tumor suppressor genes.…”

Section: Introduction: Nm23-h1 the First Metastasis Suppressormentioning

confidence: 88%

The Function of NM23-H1/NME1 and Its Homologs in Major Processes Linked to Metastasis

Mátyási

Farkas

Kopper

et al. 2020

Pathol. Oncol. Res.

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Metastasis suppressor genes (MSGs) inhibit different biological processes during metastatic progression without globally influencing development of the primary tumor. The first MSG, NM23 (non-metastatic clone 23, isoform H1) or now called NME1 (stands for nonmetastatic) was identified some decades ago. Since then, ten human NM23 paralogs forming two groups have been discovered. Group I NM23 genes encode enzymes with evolutionarily highly conserved nucleoside diphosphate kinase (NDPK) activity. In this review we summarize how results from NDPKs in model organisms converged on human NM23 studies. Next, we examine the role of NM23-H1 and its homologs within the metastatic cascade, e.g. cell migration and invasion, proliferation and apoptosis. NM23-H1 homologs are well known inhibitors of cell migration. Drosophila studies revealed that AWD, the fly counterpart of NM23-H1 is a negative regulator of cell motility by modulating endocytosis of chemotactic receptors on the surface of migrating cells in cooperation with Shibire/ Dynamin; this mechanism has been recently confirmed by human studies. NM23-H1 inhibits proliferation of tumor cells by phosphorylating the MAPK scaffold, kinase suppressor of Ras (KSR), resulting in suppression of MAPK signalling. This mechanism was also observed with the C. elegans homolog, NDK-1, albeit with an inverse effect on MAPK activation. Both NM23-H1 and NDK-1 promote apoptotic cell death. In addition, NDK-1, NM23-H1 and their mouse counterpart NM23-M1 were shown to promote phagocytosis in an evolutionarily conserved manner. In summary, inhibition of cell migration and proliferation, alongside actions in apoptosis and phagocytosis are all mechanisms through which NM23-H1 acts against metastatic progression.

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“…41 If for liver, breast, colon and lung carcinoma as well as for melanoma, the vast majority of studies reported an inverse correlation with metastasis and/or poor overall survival (Leonard et al, 91 next issue), this is less marked in gastric and ovarian carcinoma, for which disparate results were found. 88,92 In other types of cancers such as neuroblastoma, hematopoietic malignancies, and osteosarcoma, high tumoral expression was noted, which was most often correlated with poor outcome (Tan and Chang, 93 this issue). The conflicting data described in the literature, might be due, at least partially, to the presence of the two closely related isoforms NME1 and NME2, which are most often not discriminated by antibodies and probes; heterogeneous expression in the primary tumors; and/or the criteria used to evaluate and grade NME1 expression in human clinical samples.…”

Section: Nme In Metastasismentioning

confidence: 96%

The NDPK/NME superfamily: state of the art

Boissan

Schlattner

Lacombe

2018

Laboratory Investigation

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Nucleoside diphosphate kinases (NDPK) are nucleotide metabolism enzymes encoded by NME genes (also called NM23). Given the fact that not all NME-encoded proteins are catalytically active NDPKs and that NM23 generally refers to clinical studies on metastasis, we use here NME/NDPK to denote the proteins. Since their discovery in the 1950's, NMEs/NDPKs have been shown to be involved in multiple physiological and pathological cellular processes, but the molecular mechanisms have not been fully determined. Recent progress in elucidating these underlying mechanisms has been presented by experts in the field at the 10th International Congress on the NDPK/NME/AWD protein family in October 2016 in Dubrovnik, Croatia, and is summarized in review articles or original research in this and an upcoming issue of Laboratory Investigation. Within this editorial, we discuss three major cellular processes that involve members of the multi-functional NME/NDPK family: (i) cancer and metastasis dissemination, (ii) membrane remodeling and nucleotide channeling, and iii) protein histidine phosphorylation.

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NDPKA is not just a metastasis suppressor – be aware of its metastasis-promoting role in neuroblastoma

Cited by 23 publications

References 155 publications

USP7 regulates melanoma progression through PI3K/Akt/FOXO and AMPK Pathways

USP7 regulates melanoma progression through PI3K/Akt/FOXO and AMPK Pathways

The Function of NM23-H1/NME1 and Its Homologs in Major Processes Linked to Metastasis

The NDPK/NME superfamily: state of the art

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