Gene Summary

Gene:SPRR2B; small proline rich protein 2B
Databases:OMIM, HGNC, Ensembl, GeneCard, Gene
Protein:small proline-rich protein 2B
Source:NCBIAccessed: 01 September, 2019


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

Cancer Overview

Research Indicators

Publications Per Year (1994-2019)
Graph generated 01 September 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.

  • Oligonucleotide Array Sequence Analysis
  • Chromosome 1
  • Tissue Plasminogen Activator
  • Models, Genetic
  • BRINP1 protein, human
  • Lung Cancer
  • Carrier Proteins
  • Multigene Family
  • Reproducibility of Results
  • Casein Kinase Ialpha
  • Urokinase-Type Plasminogen Activator
  • Esophageal Cancer
  • Serpins
  • Poly-ADP-Ribose Binding Proteins
  • retinoic acid binding protein II, cellular
  • Lysosome-Associated Membrane Glycoproteins
  • PLAUR protein, human
  • Matrix Metalloproteinases, Membrane-Associated
  • RNA Helicases
  • DNA Helicases
  • Receptors, Scavenger
  • SCARB2 protein, human
  • Messenger RNA
  • Tumor Suppressor Proteins
  • Cancer Gene Expression Regulation
  • Bladder Cancer
  • retinoic acid binding protein I, cellular
  • Polymerase Chain Reaction
  • Squamous Cell Carcinoma
  • RNA Recognition Motif Proteins
  • Tumor Suppressor Gene
  • Gene Expression
  • Receptors, Urokinase Plasminogen Activator
  • Matrix Metalloproteinases
  • PLAT protein, human
  • Cornified Envelope Proline-Rich Proteins
  • Lymphatic Metastasis
  • Oral Cavity Cancer
  • Gene Expression Profiling
  • Skin Cancer
  • Receptors, Retinoic Acid
  • Genetic Markers
Tag cloud generated 01 September, 2019 using data from PubMed, MeSH and CancerIndex

Specific Cancers (5)

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: SPRR2B (cancer-related)

Pasini FS, Maistro S, Snitcovsky I, et al.
Four-gene expression model predictive of lymph node metastases in oral squamous cell carcinoma.
Acta Oncol. 2012; 51(1):77-85 [PubMed] Related Publications
BACKGROUND: Previous knowledge of cervical lymph node compromise may be crucial to choose the best treatment strategy in oral squamous cell carcinoma (OSCC). Here we propose a set four genes, whose mRNA expression in the primary tumor predicts nodal status in OSCC, excluding tongue.
MATERIAL AND METHODS: We identified differentially expressed genes in OSCC with and without compromised lymph nodes using Differential Display RT-PCR. Known genes were chosen to be validated by means of Northern blotting or real time RT-PCR (qRT-PCR). Thereafter we constructed a Nodal Index (NI) using discriminant analysis in a learning set of 35 patients, which was further validated in a second independent group of 20 patients.
RESULTS: Of the 63 differentially expressed known genes identified comparing three lymph node positive (pN +) and three negative (pN0) primary tumors, 23 were analyzed by Northern analysis or RT-PCR in 49 primary tumors. Six genes confirmed as differentially expressed were used to construct a NI, as the best set predictive of lymph nodal status, with the final result including four genes. The NI was able to correctly classify 32 of 35 patients comprising the learning group (88.6%; p = 0.009). Casein kinase 1alpha1 and scavenger receptor class B, member 2 were found to be up regulated in pN + group in contrast to small proline-rich protein 2B and Ras-GTPase activating protein SH3 domain-binding protein 2 which were upregulated in the pN0 group. We validated further our NI in an independent set of 20 primary tumors, 11 of them pN0 and nine pN + with an accuracy of 80.0% (p = 0.012).
CONCLUSIONS: The NI was an independent predictor of compromised lymph nodes, taking into the consideration tumor size and histological grade. The genes identified here that integrate our "Nodal Index" model are predictive of lymph node metastasis in OSCC.

Louhelainen JP, Hurst CD, Pitt E, et al.
DBC1 re-expression alters the expression of multiple components of the plasminogen pathway.
Oncogene. 2006; 25(16):2409-19 [PubMed] Related Publications
Deleted in bladder cancer 1 (DBC1) is a candidate gene for the bladder tumour suppressor locus at 9q33.1. The function of the gene is currently unknown but a cross-species sequence comparison suggests an important role, as it is highly evolutionarily conserved. Here, we transfected a nonexpressing human bladder cancer cell line with a set of human DBC1 cDNA constructs. The effect on global expression patterns was assessed using cDNA microarrays. The cell clone with the lowest level of DBC1 expression showed induced expression of 26 genes including plasminogen activator inhibitor 2 (SERPINB5; 4.6-fold), heparin-binding EGF-like growth factor precursor (DTR; 4.2-fold), small proline-rich protein 2B (SPRR2B; 3.6-fold), metallothionein 1 isoforms (MT1B/MT1A/MT-1F; from 2.9- to 3.2-fold), tissue-type plasminogen activator precursor (PLAT; 2.8-fold) and urokinase-type plasminogen activator precursor (PLAU; 2.7-fold). In clustering analysis, both PLAT and PLAU clustered with the functionally related urokinase plasminogen activator surface receptor (PLAUR; 1.9-fold). Furthermore, 14 human bladder tumours were analysed by real-time quantitative PCR using gene-specific primers for selected (n=20) genes. The expression levels of SERPINB5, PLAU, PLAUR and MT1 correlated with the DBC1 levels, suggesting previously unknown involvement of DBC1 in the urokinase-plasminogen pathway.

Tesfaigzi J, Carlson DM
Expression, regulation, and function of the SPR family of proteins. A review.
Cell Biochem Biophys. 1999; 30(2):243-65 [PubMed] Related Publications
The small, proline-rich (SPR) genes consist of three subclasses closely linked on human chromosome 1, a region referred to as the epidermal differentiation complex. SPR genes consist of two exons, with the second exon containing the entire open reading frame. SPRs are expressed in all squamous tissues of the skin, scalp, footpad, vaginal epithelia, and most of the epithelial lining of the digestive tract, including the lip, tongue, esophagus, and forestomach. Although SPR1 is absent in normal mucociliary epithelium of the respiratory tract, epithelia that undergo squamous differentiation in response to vitamin-A deficiency or to injury owing to exposure to environmental toxicants express SPR1. High levels of SPR1 are detected in various diseases and cancers of the skin or respiratory epithelia and in nonkeratinizing papillary adenocarcinomas. SPR expression can be regulated by transcriptional factors, by posttranscriptional factors, or by factors that affect SPR1 mRNA translation or protein turnover. Furthermore, regulation can be affected by the state of cell proliferation. The presence of SPR1 in most of these epithelia, and the absence of SPR3 in normal skin, suggest that these subclasses have distinct functions. Various approaches to the study of the cross-linked envelope (CE) components in identifying SPR1 and SPR2 and in suggesting that SPRs are one of the precursor proteins of the CE. However, expression of SPR1 in nonsquamous tissues and cell lines indicates a function not associated with squamous differentiation. Several studies have demonstrated that SPR1 antibodies react with nuclear proteins and that SPR1 is expressed in cells before entering the G0 phase of the cell cycle. Future studies should clarify the role of SPRs by modifying their contents in CE, and should identify SPR-associated proteins to clarify the cell growth-related role of SPR1.

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

Cite this page: Cotterill SJ. SPRR2B, Cancer Genetics Web: http://www.cancer-genetics.org/SPRR2B.htm 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: 01 September, 2019     Cancer Genetics Web, Established 1999