Gene Summary

Gene:SNX29; sorting nexin 29
Aliases: RUNDC2A, A-388D4.1
Databases:HGNC, Ensembl, GeneCard, Gene
Protein:sorting nexin-29
Source:NCBIAccessed: 31 August, 2019

Cancer Overview

Research Indicators

Publications Per Year (1994-2019)
Graph generated 31 August 2019 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.

  • Repressor Proteins
  • Carcinoma, Ovarian Epithelial
  • Chromosome 16
  • RT-PCR
  • Glandular and Epithelial Cancers
  • Cluster Analysis
  • Oligonucleotide Array Sequence Analysis
  • Gene Deletion
  • PDCD1LG2 protein, human
  • CD274 protein, human
  • Testicular Cancer
  • Chromosome Breakpoints
  • Immunohistochemistry
  • FOXP1
  • B7-H1 Antigen
  • Gene Rearrangement, B-Lymphocyte
  • Drug Resistance
  • Nuclear Proteins
  • Neoplasm Invasiveness
  • Trans-Activators
  • MHC class II transactivator protein
  • Chromosomes, Artificial, Bacterial
  • Forkhead Transcription Factors
  • Programmed Cell Death 1 Ligand 2 Protein
  • Diffuse Large B-Cell Lymphoma
  • Transcriptome
  • Ovarian Cancer
  • Translocation
  • Recurrence
  • FISH
Tag cloud generated 31 August, 2019 using data from PubMed, MeSH and CancerIndex

Specific Cancers (3)

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: SNX29 (cancer-related)

Bao F, Deng Y, Du M, et al.
Probabilistic natural mapping of gene-level tests for genome-wide association studies.
Brief Bioinform. 2018; 19(4):545-553 [PubMed] Related Publications
Genome-wide association studies (GWASs) generally focus on a single marker, which limits the elucidation of the genetic architecture of complex traits. Herein, we present a new computational framework, termed probabilistic natural mapping (PALM), for performing gene-level association tests. PALM robustly reveals the inherent genomic structures of genes and generates feature representations that can be seamlessly incorporated into conventional statistic tests. Our approach substantially improves the effectiveness of uncovering associations derived from a subgroup of variants with weak effects, which represents a known challenge associated with existing methods. We applied PALM in a gastric cancer GWAS and identified two additional gastric cancer-associated susceptibility genes, NOC3L and RUNDC2A. The robust susceptibility discoveries of PALM are widely supported by existing studies from other biological perspectives. PALM will be useful for further GWAS analytical strategies that use gene-level analyses.

Twa DD, Mottok A, Chan FC, et al.
Recurrent genomic rearrangements in primary testicular lymphoma.
J Pathol. 2015; 236(2):136-41 [PubMed] Related Publications
Primary testicular diffuse large B cell lymphoma (PTL) is an aggressive malignancy that occurs in the immune-privileged anatomical site of the testis. We have previously shown that structural genomic rearrangements involving the MHC class II transactivator CIITA and programmed death ligands (PDLs) 1 and 2 are frequent across multiple B cell lymphoma entities. Specifically in PTL, we found rearrangements in the PDL locus by fluorescence in situ hybridization (FISH). However, breakpoint anatomy and rearrangement partners were undetermined, while CIITA rearrangements had not been reported previously in PTL. Here, we performed bacterial artificial chromosome capture sequencing on three archival, formalin-fixed, paraffin-embedded tissue biopsies, interrogating 20 known rearrangement hotspots in B cell lymphomas. We report novel CIITA, FOXP1 and PDL rearrangements involving IGHG4, FLJ45248, RFX3, SMARCA2 and SNX29. Moreover, we present immunohistochemistry data supporting the association between PDL rearrangements and increased protein expression. Finally, using FISH, we show that CIITA (8/82; 10%) and FOXP1 (5/74; 7%) rearrangements are recurrent in PTL. In summary, we describe rearrangement frequencies and novel rearrangement partners of the CIITA, FOXP1 and PDL loci at base-pair resolution in a rare, aggressive lymphoma. Our data suggest immune-checkpoint inhibitor therapy as a promising intervention for PTL patients harbouring PDL rearrangements.

Zhu L, Hu Z, Liu J, et al.
Gene expression profile analysis identifies metastasis and chemoresistance-associated genes in epithelial ovarian carcinoma cells.
Med Oncol. 2015; 32(1):426 [PubMed] Free Access to Full Article Related Publications
The purpose of this study was to identify genes that associated with higher ability of metastasis and chemotherapic resistance in epithelial ovarian carcinoma (EOC) cells. An oligonucleotide microarray with probe sets complementary to 41,000(+) unique human genes and transcripts was used to determine whether gene expression profile may differentiate three epithelial ovarian cell lines (RMG-I-C, COC1 and HO8910) from their sub-lines (RMG-I-H, COCI/DDP and HO8910/PM) with higher ability of metastasis and chemotherapic resistance. Quantitative real-time PCR and immunohistochemical staining validated the microarray results. Hierarchic cluster analysis of gene expression identified 49 genes that exhibited ≥2.0-fold change and P value ≤0.05. Highly differential expression of GCET2, NLRP4, FOXP1 and SNX29 genes was validated by quantitative PCR in all cell line samples. Finally, FOXP1 was validated at the protein level by immunohistochemistry in paraffin embedded ovarian tissues (i.e., for metastasis, 15 primary EOC and 10 omental metastasis [OM]; for chemoresistance, 13 sensitive and 13 resistant EOC). The identification of higher ability of metastasis and chemotherapic resistance-associated genes may provide a foundation for the development of new type-specific diagnostic strategies and treatment for metastasis and chemotherapic resistance in epithelial ovarian cancer.

Kingston D, Chang H, Ensser A, et al.
Inhibition of retromer activity by herpesvirus saimiri tip leads to CD4 downregulation and efficient T cell transformation.
J Virol. 2011; 85(20):10627-38 [PubMed] Free Access to Full Article Related Publications
The mammalian retromer is an evolutionally conserved protein complex composed of a vacuolar protein sorting trimer (Vps 26/29/35) that participates in cargo recognition and a sorting nexin (SNX) dimer that binds to endosomal membranes. The retromer plays an important role in efficient retrograde transport for endosome-to-Golgi retrieval of the cation-independent mannose-6-phosphate receptor (CI-MPR), a receptor for lysosomal hydrolases, and other endosomal proteins. This ultimately contributes to the control of cell growth, cell adhesion, and cell migration. The herpesvirus saimiri (HVS) tyrosine kinase-interacting protein (Tip), required for the immortalization of primary T lymphocytes, targets cellular signaling molecules, including Lck tyrosine kinases and the p80 endosomal trafficking protein. Despite the pronounced effects of HVS Tip on T cell signal transduction, the details of its activity on T cell immortalization remain elusive. Here, we report that the amino-terminal conserved, glutamate-rich sequence of Tip specifically interacts with the retromer subunit Vps35 and that this interaction not only causes the redistribution of Vps35 from the early endosome to the lysosome but also drastically inhibits retromer activity, as measured by decreased levels of CI-MPR and lower activities of cellular lysosomal hydrolases. Physiologically, the inhibition of intracellular retromer activity by Tip is ultimately linked to the downregulation of CD4 surface expression and to the efficient in vitro immortalization of primary human T cells to interleukin-2 (IL-2)-independent permanent growth. Therefore, HVS Tip uniquely targets the retromer complex to impair the intracellular trafficking functions of infected cells, ultimately contributing to efficient T cell transformation.

Disclaimer: This site is for educational purposes only; it can not be used in diagnosis or treatment.

Cite this page: Cotterill SJ. RUNDC2A, Cancer Genetics Web: Accessed:

Creative Commons License
This page in Cancer Genetics Web by Simon Cotterill is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.
Note: content of abstracts copyright of respective publishers - seek permission where appropriate.

 [Home]    Page last revised: 31 August, 2019     Cancer Genetics Web, Established 1999