DNA sequences acting as binding sites for NM23/NDPK proteins in melanoma M14 cells

Cervoni, Laura; Egistelli, Lorenza; Eufemi, Margherita; d’Abusco, Anna Scotto; Altieri, Fabio; Lascu, Ioan; Turano, Carlo; Giartosio, Anna

doi:10.1002/jcb.20808

Cited by 22 publications

(23 citation statements)

References 38 publications

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“…It is likely that one or more of these transcription factors is involved in regulating the expression of NME5. As described previously, several oncosuppressor genes p53, WT1, ING1, and NM23-H1 are suggested be associated with the regulation of nm23/NDPK (Cervoni et al, 2006). In order to further characterize the NME5 promoter, truncated promoterreporter constructs were prepared.…”

Section: Discussionmentioning

confidence: 99%

Transactivation of the human NME5 gene by Sp1 in pancreatic cancer cells

Jiang

Wang

et al. 2012

Gene

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Section: Discussionmentioning

confidence: 99%

Transactivation of the human NME5 gene by Sp1 in pancreatic cancer cells

Jiang

Wang

et al. 2012

Gene

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“…Intriguingly, catalytically inactive but not wild-type NME2 has been reported to reduce metastases in melanoma (Hamby et al 2000). Analysis of NME association with chromatin in melanoma M14 cells suggested regulation of genes with crucial roles in cancer progression (Cervoni et al 2006). Together with reports in oral cancer cells showing overexpression of NME2 resulted in reduced expression of TP53, the findings suggested regulatory roles of NME2 might contribute to control of metastasis (Herak et al 2008).…”

Section: Murine Nme2 Regulates Melanoma Progressionmentioning

confidence: 89%

Mechanisms of non-metastatic 2 (NME2)-mediated control of metastasis across tumor types

Thakur

Yadav

Kumar

et al. 2011

Naunyn-Schmiedeberg's Arch Pharmacol

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Non-metastatic 23 [NM23/nucleoside diphosphate kinases (NDPK)] genes are the first discovered metastasis suppressor genes. More than two decades of research has demonstrated their roles in a variety of biological processes with NME1 and NME2 being most studied in the context of metastasis suppression. Although NME1 and NME2 share >85% homology at amino acid level, they show redundant as well as unique molecular functions. Phenotypic analyses of knockout (KO) mice for NM23 members (NDPK-A, B) and compound KO (A as well as B) showed requirement of both proteins in hematopoiesis suggesting shared functions in development disease. Several reviews have discussed NME1, however the role of NME2 appears to be relatively less understood in the context of metastasis suppression. Here, we focus on NME2 and by meta-analysis of gene expression from multiple tumor types, and survey of in vivo and vitro studies, suggest the possibility that NME2 may be one of the key factors in metastasis. This along with the relevance of normal physiological functions of NME2 in the context of metastasis is discussed. We further examined the genetic and epigenetic features of NME2 and NME1 gene promoters and found aspects of transcription control that could be unique to NME2/NME1. Findings on signaling pathways and small molecules which regulate the expression of NME2 that could be therapeutically important are also discussed.

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“…The exogenous expression of nm23-H1 in cells without endogenous nm23-H1 expression not only suppresses migration and invasion but also decreases cell proliferation and anchorage-independent growth (Jung et al, 2006;McDermott et al, 2008). Moreover, nm23-H1 protein inhibits telomerase activity (Kar et al, 2012) and increases cell-cell adhesion (Bago et al, 2009), cell-cycle arrest, and apoptosis (Cervoni et al, 2006). This suggests that nm23-H1 plays an important role in the process of tumor formation and metastasis.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of invasion and metastasis of human liver cancer HCCLM3 cells by portulacerebroside A

Qian¹,

Zheng²,

Chen³

et al. 2014

Pharmaceutical Biology

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Objective: This study investigates the effects of PCA in human liver cancer HCCLM3 cells on metastasis and invasion. Materials and methods: After the cells were treated with PCA (2.5, 5, and 10 mg/ml) for 6, 12, 24, or 48 h, adhesion, transwell invasion, and scratch tests were conducted and cell functions were evaluated. Western blot and FQ-RT-PCR assays explored the mechanism of PCA-inhibited invasion and metastasis in the cells. Results:The adhesion rate of the cells was suppressed at 0.5 h (79.4 ± 1.0, 68.7 ± 1.3, and 58.1 ± 1.3%, versus 100 ± 1.5% in the control), 1 h (78.2 ± 1.2, 70.9 ± 1.6, and 55.4 ± 1.9%, versus 100 ± 1.2% in the control), and 1.5 h (71.6 ± 1.1, 62.3 ± 0.9, and 50.4 ± 0.9%, versus 100 ± 1.1% in the control). The 24 h invasion ability was decreased (356.6 ± 11.2, 204.0 ± 17.6, and 113.0 ± 9.5%, versus 443.6 ± 15.4% in the control). The migration capability was also restrained by PCA for 24 h (324.8 ± 25.4, 250.4 ± 21.0, and 126.3 ± 10.1, versus 381.6 ± 30.6 in the control) and 48 h (470.3 ± 34.3, 404.0 ± 19.7, and 201.0 ± 15.4, versus 752.0 ± 63.6 in the control). There was an increase in the mRNA and protein expression levels of TIMP-2 and nm23-H1, inhibition in the mRNA expression of MTA1, MMP-2, and MMP-9, and suppression in the protein expression of MTA1, RhoA, Rac1/Cdc42, MMP-2, but not RhoC and MMP-9. Conclusion: PCA suppresses the invasion and metastasis of HCCLM3 cells possibly by modulation of the mRNA and protein expression of related parameters. This is the first study to reveal a new potential therapeutic application of PCA in antimetastatic therapy for liver cancer.

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DNA sequences acting as binding sites for NM23/NDPK proteins in melanoma M14 cells

Cited by 22 publications

References 38 publications

Transactivation of the human NME5 gene by Sp1 in pancreatic cancer cells

Transactivation of the human NME5 gene by Sp1 in pancreatic cancer cells

Mechanisms of non-metastatic 2 (NME2)-mediated control of metastasis across tumor types

Inhibition of invasion and metastasis of human liver cancer HCCLM3 cells by portulacerebroside A

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