PDCD7

Gene Summary

Gene:PDCD7; programmed cell death 7
Aliases: ES18, HES18
Location:15q22.31
Summary:This gene encodes a 59 kDa protein that is associated with the U11 small nuclear ribonucleoprotein (snRNP), which is a component of the minor U12-type spliceosome responsible for catalyzing pre-mRNA splicing of U12-type introns. [provided by RefSeq, Dec 2010]
Databases:VEGA, OMIM, HGNC, Ensembl, GeneCard, Gene
Protein:programmed cell death protein 7
Source:NCBIAccessed: 11 March, 2017

Ontology:

What does this gene/protein do?
Show (5)

Cancer Overview

Research Indicators

Publications Per Year (1992-2017)
Graph generated 11 March 2017 using data from PubMed using criteria.

Literature Analysis

Mouse over the terms for more detail; many indicate links which you can click for dedicated pages about the topic.

  • Lectins, C-Type
  • Microtubule-Associated Proteins
  • DNA-Binding Proteins
  • Adolescents
  • Gene Expression Profiling
  • Apoptosis Regulatory Proteins
  • NIH 3T3 Cells
  • RTPCR
  • Reproducibility of Results
  • C11orf2
  • Nuclear Proteins
  • Cytogenetic Analysis
  • DNA Damage
  • Multivariate Analysis
  • PDCD7
  • Young Adult
  • Transcription Factors
  • Membrane Proteins
  • Gene Knockdown Techniques
  • Receptors, Natural Killer Cell
  • Cancer Gene Expression Regulation
  • Acute Myeloid Leukaemia
  • KLRF1
  • Leukemic Gene Expression Regulation
  • PDRG1
  • FIS1
  • Case-Control Studies
  • Mitochondrial Proteins
  • Chromosome 15
  • MAP1S
  • Oligonucleotide Array Sequence Analysis
  • Recurrence
  • Biomarkers, Tumor
  • Immunoblotting
  • Vesicular Transport Proteins
  • Ciz1
Tag cloud generated 11 March, 2017 using data from PubMed, MeSH and CancerIndex

Specific Cancers (1)

Data table showing topics related to specific cancers and associated disorders. Scope includes mutations and abnormal protein expression.

Note: list is not exhaustive. Number of papers are based on searches of PubMed (click on topic title for arbitrary criteria used).

Latest Publications: PDCD7 (cancer-related)

Zhang D, Li Y, Wang R, et al.
Inhibition of REST Suppresses Proliferation and Migration in Glioblastoma Cells.
Int J Mol Sci. 2016; 17(5) [PubMed] Free Access to Full Article Related Publications
Glioblastoma (GBM) is the most common primary brain tumor, with poor prognosis and a lack of effective therapeutic options. The aberrant expression of transcription factor REST (repressor element 1-silencing transcription factor) had been reported in different kinds of tumors. However, the function of REST and its mechanisms in GBM remain elusive. Here, REST expression was inhibited by siRNA silencing in U-87 and U-251 GBM cells. Then CCK-8 assay showed significantly decreased cell proliferation, and the inhibition of migration was verified by scratch wound healing assay and transwell assay. Using cell cycle analysis and Annexin V/PI straining assay, G1 phase cell cycle arrest was found to be a reason for the suppression of cell proliferation and migration upon REST silencing, while apoptosis was not affected by REST silencing. Further, the detection of REST-downstream genes involved in cytostasis and migration inhibition demonstrated that CCND1 and CCNE1 were reduced; CDK5R1, BBC3, EGR1, SLC25A4, PDCD7, MAPK11, MAPK12, FADD and DAXX were enhanced, among which BBC3 and DAXX were direct targets of REST, as verified by ChIP (chromatin immunoprecipitation) and Western blotting. These data suggested that REST is a master regulator that maintains GBM cells proliferation and migration, partly through regulating cell cycle by repressing downstream genes, which might represent a potential target for GBM therapy.

Tian Y, Huang Z, Wang Z, et al.
Identification of novel molecular markers for prognosis estimation of acute myeloid leukemia: over-expression of PDCD7, FIS1 and Ang2 may indicate poor prognosis in pretreatment patients with acute myeloid leukemia.
PLoS One. 2014; 9(1):e84150 [PubMed] Free Access to Full Article Related Publications
Numerous factors impact on the prognosis of acute myeloid leukemia (AML), among which molecular genetic abnormalities are developed increasingly, however, accurate prediction for newly diagnosed AML patients remains unsatisfied. For further improving the prognosis evaluation system, we investigated the transcripts levels of PDCD7, FIS1, FAM3A, CA6, APP, KLRF1, ATCAY, GGT5 and Ang2 in 97 AML patients and 30 non-malignant controls, and validated using the published microarray data from 225 cytogenetically normal AML (CN-AML) patients treated according to the German AMLCG-1999 protocol. Real-time quantitative polymerase chain reaction and western blot were carried out, and clinical data were collected and analyzed. High Ang2 and FIS1 expression discriminated the CR rate of AML patients (62.5% versus 82.9% for Ang2, P = 0.011; 61.4% versus 82.2% for FIS1, P = 0.029). In CN-AML, patients with high FIS1 expression were more likely to be resistant to two courses of induction (P = 0.035). Overall survival (OS) and relapse-free survival (RFS) were shorter in CN-AML patients with high PDCD7 expression (P<0.001; P = 0.006), and PDCD7 was revealed to be an independent risk factor for OS in CN-AML (P = 0.004). In the analysis of published data from 225 CN-AML patients, PDCD7 remained independently predicting OS in CN-AML (P = 0.039). As a conclusion, Ang2 and FIS1 seem related to decreased CR rate of AML patients, and PDCD7 is associated with shorter OS and RFS in CN-AML. Hence, PDCD7, Ang2 and FIS1 may indicate a more aggressive form and poor prognosis of AML.

Jiang L, Luo X, Shi J, et al.
PDRG1, a novel tumor marker for multiple malignancies that is selectively regulated by genotoxic stress.
Cancer Biol Ther. 2011; 11(6):567-73 [PubMed] Free Access to Full Article Related Publications
We have previously cloned and characterized a novel p53 and DNA damage-regulated gene named PDRG1. PDRG1 was found to be differentially regulated by ultraviolet (UV) radiation and p53. In this study, we further investigated stress regulation of PDRG1 and found it to be selectively regulated by agents that induce genotoxic stress (DNA damage). Using cancer profiling arrays, we also investigated PDRG1 expression in matching normal and tumor samples representing various malignancies and found its expression to be upregulated in multiple malignancies including cancers of the colon, rectum, ovary, lung, stomach, breast and uterus when compared to their respective matched normal tissues. Western blot and immunohistochemical analyses were also performed on select specimen sets of colon cancers and matching normal tissues and the results also indicated PDRG1 overexpression in tumors relative to normal tissues. To gain insight into the function of PDRG1, we performed PDRG1 knockdown in human colon cancer cells and found its depletion to result in marked slowdown of tumor cell growth. These results suggest that PDGR1 may be linked to cell growth regulation. Yeast two-hybrid screen also led to the identification of PDCD7, CIZ1 and MAP1S as PDRG1-interacting proteins that are involved in apoptosis and cell cycle regulation which further implicate PDRG1 in controlling cell growth regulation. Taken together, our results indicate that PDRG1 expression is increased in multiple human malignancies suggesting it to be a high-value novel tumor marker that could play a role in cancer development and/or progression.

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Cite this page: Cotterill SJ. PDCD7, Cancer Genetics Web: http://www.cancer-genetics.org/PDCD7.htm Accessed:

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This page in Cancer Genetics Web by Simon Cotterill is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.
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