Unc5D regulates p53-dependent apoptosis in neuroblastoma cells

Wang, Hong; Wu, Qiong; Li, Shuang; Zhang, Bin; Chi, Zuofei; Hao, Liangchun

doi:10.3892/mmr.2014.2100

Cited by 14 publications

(17 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Epigenetic changes are common features of PCa, and play key roles in the initiation and progression of cancer . As for UNC5D , hypermethylation alterations at the promoter region are one of the main causes for its repression in a variety of tumors, and are the same in PCa cells according to our study. However, there are seldom reports on the methylation status of UNC5D in metastatic tumors.…”

Section: Discussionsupporting

confidence: 60%

“…UNC5D/H4 is the most recently identified member of UNC5 family . Like other members of this family, UNC5D has also been characterized as a tumor suppressor gene in several cancers, such as neuroblastoma, renal cell carcinoma, and bladder cancer . UNC5D has been observed with high expression in the human prostate tissue, but underexpressed in the castration‐resistant stage of prostate cancer .…”

Section: Introductionmentioning

confidence: 99%

“…10,12,13 UNC5D/H4 is the most recently identified member of UNC5 family. 14 Like other members of this family, UNC5D has also been characterized as a tumor suppressor gene in several cancers, such as neuroblastoma, 15,16 renal cell carcinoma, 17 and bladder cancer. 18…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

UNC5D, suppressed by promoter hypermethylation, inhibits cell metastasis by activating death‐associated protein kinase 1 in prostate cancer

et al. 2019

View full text Add to dashboard Cite

Prostate cancer ( PC a) death primarily occurs due to metastasis of the cells, but little is known about the underlying molecular mechanisms. This study aimed to evaluate the expression of UNC 5D , a newly identified tumor suppressor gene, analyze its epigenetic alterations, and elucidate its functional relevance to PC a metastasis. Meta‐analysis of publicly available microarray datasets revealed that UNC 5D expression was frequently downregulated in PC a tissues and inversely associated with PC a metastasis. These results were verified in clinical specimens by real‐time PCR and immunohistochemistry assays. Through methylation analysis, the downregulated expression of UNC 5D in PC a tissues and cell lines was found to be attributable to the hypermethylation of the promoter. A negative correlation was observed between methylation and UNC 5D mRNA expression in PC a samples. The ectopic expression of UNC 5D in PC a cells effectively reduced their ability to migrate and invade both in vitro and in vivo, and si RNA ‐mediated knockdown of UNC 5D yielded consistent results. UNC 5D can recruit and activate death‐associated protein kinase 1, which remained to be essential for its metastatic suppressor function. In conclusion, these results suggested that UNC 5D as a novel putative metastatic suppressor gene that is commonly down‐regulated by hypermethylation in PC a.

show abstract

Section: Discussionsupporting

confidence: 60%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

UNC5D, suppressed by promoter hypermethylation, inhibits cell metastasis by activating death‐associated protein kinase 1 in prostate cancer

et al. 2019

View full text Add to dashboard Cite

show abstract

“…We found a deletion of UNC5D in a child with focal epilepsy, mesiotemporal sclerosis and developmental and behavioral problems, as well as in his father who had migraine. UNC5D (MIM 616466) on chromosome 8p12 has been shown to be involved in cortical development and p53‐dependent apoptosis in neuroblastoma cells . UNC5D was considered as a candidate gene for neurodevelopmental phenotypes in a family with a t(6;8) balanced translocation that disrupted this gene in two affected siblings with developmental delay (one with schizencephaly) and their asymptomatic mother .…”

Section: Discussionmentioning

confidence: 99%

Copy number variation in a hospital‐based cohort of children with epilepsy

et al. 2017

View full text Add to dashboard Cite

SummaryObjectiveTo evaluate the diagnostic yield of microarray analysis in a hospital‐based cohort of children with seizures and to identify novel candidate genes and susceptibility loci for epilepsy.MethodsOf all children who presented with their first seizure in the University Medical Center Groningen (January 2000 through May 2013) (n = 1,368), we included 226 (17%) children who underwent microarray analysis before June 2014. All 226 children had a definite diagnosis of epilepsy. All their copy number variants (CNVs) on chromosomes 1–22 and X that contain protein‐coding genes and have a prevalence of <1% in healthy controls were evaluated for their pathogenicity.ResultsChildren selected for microarray analysis more often had developmental problems (82% vs. 25%, p < 0.001), facial dysmorphisms (49% vs. 8%, p < 0.001), or behavioral problems (41% vs. 13%, p < 0.001) than children who were not selected. We found known clinically relevant CNVs for epilepsy in 24 of the 226 children (11%). Seventeen of these 24 children had been diagnosed with symptomatic focal epilepsy not otherwise specified (71%) and five with West syndrome (21%). Of these 24 children, many had developmental problems (100%), behavioral problems (54%) or facial dysmorphisms (46%). We further identified five novel CNVs comprising four potential candidate genes for epilepsy: MYT1L, UNC5D, SCN4B, and NRXN3.SignificanceThe 11% yield in our hospital‐based cohort underscores the importance of microarray analysis in diagnostic evaluation of children with epilepsy.

show abstract

“…78 Phenylarsonous acid analogs bind and causes degradation of the fusion protein PML/RAR-alpha. 79 UNC5H4 is a direct transcriptional target of p53. 80 PML interacts with Fas.…”

Section: Network Analysis Of Selected Proteinsmentioning

confidence: 99%

Bioinformatics Predictions of Fas Related Protein Network

WeijunGuan

2016

j comput theor nanosci

View full text Add to dashboard Cite

Fas is a cell surface receptor that, when engaged by Fas ligand (FasL) or specific agonistic antibodies, triggers apoptosis. Binding of an adaptor protein, FADD, to the death-effector domain of Fas activates a cascade of cysteine proteases known as caspases that cleave cellular substrates, resulting in cell death. The aim of this study was to systematically construct the global proteinprotein interaction (PPI) network and predict Fas related protein connections by network analysis using MetaCore.

show abstract

Unc5D regulates p53-dependent apoptosis in neuroblastoma cells

Cited by 14 publications

References 18 publications

UNC5D, suppressed by promoter hypermethylation, inhibits cell metastasis by activating death‐associated protein kinase 1 in prostate cancer

UNC5D, suppressed by promoter hypermethylation, inhibits cell metastasis by activating death‐associated protein kinase 1 in prostate cancer

Copy number variation in a hospital‐based cohort of children with epilepsy

Bioinformatics Predictions of Fas Related Protein Network

Contact Info

Product

Resources

About