Visinin-like protein-1 is a potent inhibitor of cell adhesion and migration in squamous carcinoma cells

Guerrico, Anatilde M. Gonzalez; Jaffer, Zahara M.; Page, Robert E.; Braunewell, Karl-Heinz; Chernoff, Jonathan; Klein‐Szanto, Andres J.

doi:10.1038/sj.onc.1208476

Cited by 36 publications

(47 citation statements)

References 36 publications

(30 reference statements)

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“…The present data also indicated that some genes (such as VSNL1 in NB cell lines, and PQLC3 in both SCLC and NB cell lines) are consistently down-regulated regardless of their amplification status. VSNL1 down-regulation has been already reported in squamous carcinoma cells (Gonzalez Guerrico et al 2005) and in non-small cell lung carcinomas (Fu et al 2008). Our data suggest that it may have a tumor suppressor role also in NB tumors.…”

Section: Double Minutes and Hsr In Solid Tumorssupporting

confidence: 55%

Gene amplification as double minutes or homogeneously staining regions in solid tumors: Origin and structure

Storlazzi¹,

Lonoce²,

et al. 2010

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Double minutes (dmin) and homogeneously staining regions (hsr) are the cytogenetic hallmarks of genomic amplification in cancer. Different mechanisms have been proposed to explain their genesis. Recently, our group showed that the MYC-containing dmin in leukemia cases arise by excision and amplification (episome model). In the present paper we investigated 10 cell lines from solid tumors showing MYCN amplification as dmin or hsr. Particularly revealing results were provided by the two subclones of the neuroblastoma cell line STA-NB-10, one showing dmin-only and the second hsr-only amplification. Both subclones showed a deletion, at 2p24.3, whose extension matched the amplicon extension. Additionally, the amplicon structure of the dmin and hsr forms was identical. This strongly argues that the episome model, already demonstrated in leukemias, applies to solid tumors as well, and that dmin and hsr are two faces of the same coin. The organization of the duplicated segments varied from very simple (no apparent changes from the normal sequence) to very complex. MYCN was always overexpressed (significantly overexpressed in three cases). The fusion junctions, always mediated by nonhomologous end joining, occasionally juxtaposed truncated genes in the same transcriptional orientation. Fusion transcripts involving NBAS (also known as NAG), FAM49A, BC035112 (also known as NCRNA00276), and SMC6 genes were indeed detected, although their role in the context of the tumor is not clear.

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Section: Double Minutes and Hsr In Solid Tumorssupporting

confidence: 55%

Gene amplification as double minutes or homogeneously staining regions in solid tumors: Origin and structure

Storlazzi¹,

Lonoce²,

et al. 2010

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“…Basal epidermal keratinocytes of normal murine skin express VILIP-1, whereas its expression is markedly decreased in aggressive and invasive squamous cell carcinomas (8). Enforced expression of VILIP-1 led to inhibition of cell adhesion and migration by down-regulating fibronectin receptors, suggesting a tumor suppressor function for VILIP-1 (9). Similarly, VILIP-1 expression is present in normal squamous epithelium of esophagus and bronchial mucociliary epithelium.…”

Section: Vilip-1mentioning

confidence: 86%

Promoter Regulation of the Visinin-like Subfamily of Neuronal Calcium Sensor Proteins by Nuclear Respiratory Factor-1

Zhang

Jin

et al. 2009

Journal of Biological Chemistry

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VILIP-1 (gene name VSNL1), a member of the neuronal Ca 2؉sensor protein family, acts as a tumor suppressor gene by inhibiting cell proliferation, adhesion, and invasiveness. VILIP-1 expression is down-regulated in several types of human cancer. In human non-small cell lung cancer, we found that down-regulation was due to epigenetic changes. Consequently, in this study we analyzed the VSNL1 promoter and its regulation. Serial truncation of the proximal 2-kb VSNL1 promoter (VP-1998) from its 5 terminus disclosed that the last 3 terminal 100-bp promoter fragment maintained similar promoter activity as compared with VP-1998 and therefore was referred to as VSNL1 minimal promoter. When the 5 terminal 50 bp were deleted from the minimal promoter, the activity was dramatically decreased, suggesting that the deleted 50 bp contained a potential cis-acting element crucial for promoter activity. Deletion and site-directed mutagenesis combined with in silico transcription factor binding analysis of VSNL1 promoter identified nuclear respiratory factor (NRF)-1/␣-PAL as a major player in regulating VSNL1 minimal promoter activity. The function of NRF-1 was further confirmed using dominant-negative NRF-1 overexpression and NRF-1 small interfering RNA knockdown. Electrophoretic mobility shift assay and chromatin immunoprecipitation provided evidence for direct NRF-1 binding to the VSNL1 promoter. Methylation of the NRF-1-binding site was found to be able to regulate VSNL1 promoter activity. Our results further indicated that NRF-1 could be a regulatory factor for gene expression of the other visininlike subfamily members including HPCAL4, HPCAL1, HPCA, and NCALD.

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“…Previous results suggest VSNL1 regulates heart natriuretic peptide receptor B [93]. The VSNL1 gene also plays a critical role in regulating cell adhesion and migration via downregulation of fibronectin receptor expression [95]. The VSNL1 gene is highly expressed in the nervous system.…”

Section: Discussionmentioning

confidence: 99%

Detection of genome-wide copy number variations in two chicken lines divergently selected for abdominal fat content

Zhang

Dong

et al. 2014

BMC Genomics

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BackgroundThe chicken (Gallus gallus) is an important model organism that bridges the evolutionary gap between mammals and other vertebrates. Copy number variations (CNVs) are a form of genomic structural variation widely distributed in the genome. CNV analysis has recently gained greater attention and momentum, as the identification of CNVs can contribute to a better understanding of traits important to both humans and other animals. To detect chicken CNVs, we genotyped 475 animals derived from two broiler chicken lines divergently selected for abdominal fat content using chicken 60 K SNP array, which is a high-throughput method widely used in chicken genomics studies.ResultsUsing PennCNV algorithm, we detected 438 and 291 CNVs in the lean and fat lines, respectively, corresponding to 271 and 188 CNV regions (CNVRs), which were obtained by merging overlapping CNVs. Out of these CNVRs, 99% were confirmed also by the CNVPartition program. These CNVRs covered 40.26 and 30.60 Mb of the chicken genome in the lean and fat lines, respectively. Moreover, CNVRs included 176 loss, 68 gain and 27 both (i.e. loss and gain within the same region) events in the lean line, and 143 loss, 25 gain and 20 both events in the fat line. Ten CNVRs were chosen for the validation experiment using qPCR method, and all of them were confirmed in at least one qPCR assay. We found a total of 886 genes located within these CNVRs, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses showed they could play various roles in a number of biological processes. Integrating the results of CNVRs, known quantitative trait loci (QTL) and selective sweeps for abdominal fat content suggested that some genes (including SLC9A3, GNAL, SPOCK3, ANXA10, HELIOS, MYLK, CCDC14, SPAG9, SOX5, VSNL1, SMC6, GEN1, MSGN1 and ZPAX) may be important for abdominal fat deposition in the chicken.ConclusionsOur study provided a genome-wide CNVR map of the chicken genome, thereby contributing to our understanding of genomic structural variations and their potential roles in abdominal fat content in the chicken.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2164-15-517) contains supplementary material, which is available to authorized users.

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Visinin-like protein-1 is a potent inhibitor of cell adhesion and migration in squamous carcinoma cells

Cited by 36 publications

References 36 publications

Gene amplification as double minutes or homogeneously staining regions in solid tumors: Origin and structure

Gene amplification as double minutes or homogeneously staining regions in solid tumors: Origin and structure

Promoter Regulation of the Visinin-like Subfamily of Neuronal Calcium Sensor Proteins by Nuclear Respiratory Factor-1

Detection of genome-wide copy number variations in two chicken lines divergently selected for abdominal fat content

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