Gene Summary

Gene:THRAP3; thyroid hormone receptor associated protein 3
Aliases: TRAP150
Databases:OMIM, VEGA, HGNC, Ensembl, GeneCard, Gene
Protein:thyroid hormone receptor-associated protein 3
Source:NCBIAccessed: 17 August, 2015


What does this gene/protein do?
Show (17)

Cancer Overview

Research Indicators

Publications Per Year (1990-2015)
Graph generated 17 August 2015 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.

  • Cancer DNA
  • Cancer RNA
  • Virus Integration
  • Cancer Gene Expression Regulation
  • Protein Kinases
  • Cyclin D1
  • Insertional Mutagenesis
  • THRAP3
  • Cell Cycle
  • Gene Rearrangement
  • CNBP
  • Proteoglycans
  • Polymerase Chain Reaction
  • Ribosomal Proteins
  • Up-Regulation
  • beta-galactoside alpha-2,3-sialyltransferase
  • MTOR
  • Neoplastic Cell Transformation
  • Tumor Markers
  • Base Sequence
  • Parathyroid Cancer
  • Single Nucleotide Polymorphism
  • siRNA
  • Transfection
  • Sialyltransferases
  • ITPR1
  • Chromosome 1
  • Neoplasm Recurrence, Local
  • Genomics
  • Bone Cancer
  • Sarcoplasmic Reticulum Calcium-Transporting ATPases
  • Nucleic Acid Amplification Techniques
  • Calcium-Transporting ATPases
  • DNA-Binding Proteins
  • Transcription Factors
  • TOR Serine-Threonine Kinases
  • HeLa Cells
  • ITPR2
  • Neoplasm Proteins
  • Transcription
Tag cloud generated 17 August, 2015 using data from PubMed, MeSH and CancerIndex

Specific Cancers (2)

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: THRAP3 (cancer-related)

Kasaian K, Wiseman SM, Thiessen N, et al.
Complete genomic landscape of a recurring sporadic parathyroid carcinoma.
J Pathol. 2013; 230(3):249-60 [PubMed] Related Publications
Parathyroid carcinoma is a rare endocrine malignancy with an estimated incidence of less than 1 per million population. Excessive secretion of parathyroid hormone, extremely high serum calcium level, and the deleterious effects of hypercalcaemia are the clinical manifestations of the disease. Up to 60% of patients develop multiple disease recurrences and although long-term survival is possible with palliative surgery, permanent remission is rarely achieved. Molecular drivers of sporadic parathyroid carcinoma have remained largely unknown. Previous studies, mostly based on familial cases of the disease, suggested potential roles for the tumour suppressor MEN1 and proto-oncogene RET in benign parathyroid tumourigenesis, while the tumour suppressor HRPT2 and proto-oncogene CCND1 may also act as drivers in parathyroid cancer. Here, we report the complete genomic analysis of a sporadic and recurring parathyroid carcinoma. Mutational landscapes of the primary and recurrent tumour specimens were analysed using high-throughput sequencing technologies. Such molecular profiling allowed for identification of somatic mutations never previously identified in this malignancy. These included single nucleotide point mutations in well-characterized cancer genes such as mTOR, MLL2, CDKN2C, and PIK3CA. Comparison of acquired mutations in patient-matched primary and recurrent tumours revealed loss of PIK3CA activating mutation during the evolution of the tumour from the primary to the recurrence. Structural variations leading to gene fusions and regions of copy loss and gain were identified at a single-base resolution. Loss of the short arm of chromosome 1, along with somatic missense and truncating mutations in CDKN2C and THRAP3, respectively, provides new evidence for the potential role of these genes as tumour suppressors in parathyroid cancer. The key somatic mutations identified in this study can serve as novel diagnostic markers as well as therapeutic targets.

Cha JD, Kim HJ, Cha IH
Genetic alterations in oral squamous cell carcinoma progression detected by combining array-based comparative genomic hybridization and multiplex ligation-dependent probe amplification.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2011; 111(5):594-607 [PubMed] Related Publications
BACKGROUND: Oral squamous cell carcinoma (OSCC), the most common malignancy of the oral cavity, has been shown to occur via a multistep process driven by the accumulation of carcinogen-induced genetic changes.
STUDY DESIGN: Array-based comparative genomic hybridization (aCGH) and multiplex ligation-dependent probe amplification (MLPA) were conducted to screen human genomewide alterations on fresh tissues of the cancer area, the dysplastic transitional area, and the resection margin (normal) free of tumor; these samples were obtained from 7 OSCC patients.
RESULTS: The highest amplification frequencies (100%, 7/7) were detected in FAM5B, TIPARP, PIK3CA, NLGN1, FGF10, HDAC9, GRM3, DDEF1, EDNRB, CHRDL1, and HTR2C, and the highest deletion frequencies in THRAP3, CTTNBP2NL, GATAD2B, REL, CKAP2L, RHOA, EIF4E3, PDLIM5, FBXO3, NEUROD4, and ABCA5 in the OSCC. In the dysplasia, amplification (100%, 7/7) was detected in RNF36 and deletion in CKAP2L and TCF8. We could detect large differences with MLPA in the number of alterations between the cancer or dysplasia versus the normal area with P values of <.001.
CONCLUSION: These findings indicate that these DNA copy number changes on each chromosome in the 3 categories may be associated with OSCC tumorigenesis and/or progression.

Bracken CP, Wall SJ, Barré B, et al.
Regulation of cyclin D1 RNA stability by SNIP1.
Cancer Res. 2008; 68(18):7621-8 [PubMed] Free Access to Full Article Related Publications
Cyclin D1 expression represents one of the key mitogen-regulated events during the G(1) phase of the cell cycle, whereas Cyclin D1 overexpression is frequently associated with human malignancy. Here, we describe a novel mechanism regulating Cyclin D1 levels. We find that SNIP1, previously identified as a regulator of Cyclin D1 expression, does not, as previously thought, primarily function as a transcriptional coactivator for this gene. Rather, SNIP1 plays a critical role in cotranscriptional or posttranscriptional Cyclin D1 mRNA stability. Moreover, we show that the majority of nucleoplasmic SNIP1 is present within a previously undescribed complex containing SkIP, THRAP3, BCLAF1, and Pinin, all proteins with reported roles in RNA processing and transcriptional regulation. We find that this complex, which we have termed the SNIP1/SkIP-associated RNA-processing complex, is coordinately recruited to both the 3' end of the Cyclin D1 gene and Cyclin D1 RNA. Significantly, SNIP1 is required for the further recruitment of the RNA processing factor U2AF65 to both the Cyclin D1 gene and RNA. This study shows a novel mechanism regulating Cyclin D1 expression and offers new insight into the role of SNIP1 and associated proteins as regulators of proliferation and cancer.

Oliveira AM, Perez-Atayde AR, Dal Cin P, et al.
Aneurysmal bone cyst variant translocations upregulate USP6 transcription by promoter swapping with the ZNF9, COL1A1, TRAP150, and OMD genes.
Oncogene. 2005; 24(21):3419-26 [PubMed] Related Publications
Aneurysmal bone cysts (ABC) are locally aggressive bone tumors that often feature chromosome 17p13 rearrangements. One of the ABC 17p13 rearrangements--t(16;17)(q22;p13)--was recently shown to create a CDH11-USP6 fusion in which the USP6/TRE17 oncogene is overexpressed through juxtaposition with the CDH11 promoter. Herein, we characterize four different ABC translocations involving 17p13, and we show that each is associated with a novel USP6 fusion oncogene. Specifically, we demonstrate that t(1;17), t(3;17), t(9;17), and t(17;17) result in USP6 fusions with TRAP150 (thyroid receptor-associated protein 150), ZNF9 (ZiNc Finger 9), Osteomodulin, and COL1A1 (Collagen 1A1), respectively. The oncogenic mechanism in these fusion genes is akin to CDH11-USP6, with the USP6 coding sequences juxtaposed to the promoter regions in each of the four novel translocation partners. The novel fusion partners appear well suited to drive USP6 transcription in the bone/mesenchymal context: osteomodulin is expressed strongly in osteoblastic lineages, and the COL1A1 promoter has an oncogenic role in the mesenchymal cancer dermatofibrosarcoma protuberans. In summary, these studies show that USP6 oncogenic activation results from heterogeneous genomic mechanisms involving USP6 transcriptional upregulation by juxtaposition with ectopic promoters.

Paterlini-Bréchot P, Saigo K, Murakami Y, et al.
Hepatitis B virus-related insertional mutagenesis occurs frequently in human liver cancers and recurrently targets human telomerase gene.
Oncogene. 2003; 22(25):3911-6 [PubMed] Related Publications
Integration of Hepatitis B Virus (HBV) DNA into liver cell DNA has been well established, but its implication in liver carcinogenesis is still being debated. In particular, insertion of the viral genome into cellular genes has been viewed as a rare event. By using HBV-Alu PCR, we have now isolated, from nine hepatocellular carcinomas, nine HBV-DNA integration sites showing that the viral genome mutates key regulatory cellular genes: neurotropic tyrosin receptor kinase 2 (NTRK2) gene, IL-1R-associated kinase 2 (IRAK2) gene, p42 mitogen-activated protein kinase 1 (p42MAPK1) gene, inositol 1,4,5-triphosphate receptor type 2 (IP3R2) gene, inositol 1,4,5-triphosphate receptor (IP3R) type 1 (IP3R1) gene, alpha 2,3 sialyltransferase (ST3GAL VI or SITA) gene, thyroid hormone uncoupling protein (TRUP) gene, EMX2-like gene, and human telomerase reverse transcriptase (hTERT) gene. This result brings to 15 the total number of genes targeted by HBV in a study of 22 human liver cancers. Overall, we found that both the inositol 1,4,5-triphosphate receptor gene and the telomerase gene were targeted by HBV in two different tumors. Thus, HBV frequently targets cellular genes involved in cell signalling and some of them may be preferential targets of the viral integration.

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Cite this page: Cotterill SJ. THRAP3, Cancer Genetics Web: Accessed:

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