TC-1 Is a Novel Tumorigenic and Natively Disordered Protein Associated with Thyroid Cancer

Sunde, Margaret; McGrath, Kristine; Young, L. S.; Matthews, Jacqueline M.; Chua, Elizabeth L.; Mackay, Joel P.; Death, Alison K.

doi:10.1158/0008-5472.can-03-2093

Cited by 71 publications

(82 citation statements)

References 45 publications

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“…Recent data from other laboratories also are not consistent with an oncogenic role for TACC1 in breast cancer and suggest it to be a candidate tumor suppressor gene from this genomic region (40). C8orf4, by contrast, seems to be overexpressed in a high proportion of breast cancers as well as thyroid and gastric cancer, regardless of copy number status (41,42).…”

Section: Discussionmentioning

confidence: 85%

Multiple Interacting Oncogenes on the 8p11-p12 Amplicon in Human Breast Cancer

Yang¹,

Streicher²,

et al. 2006

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The 8p11-p12 genomic region is amplified in 15% of breast cancers and harbors several candidate oncogenes. However, functional evidence for a transforming role for these genes is lacking. We identified 21 genes from this region as potential oncogenes based on statistical association between copy number and expression. We further showed that three of these genes (LSM1, BAG4, and C8orf4) induce transformed phenotypes when overexpressed in MCF-10A cells, and overexpression of these genes in combination influences the growth factor independence phenotype and the ability of the cells to grow under anchorage-independent conditions. Thus, LSM1, BAG4, and C8orf4 are breast cancer oncogenes that can work in combination to influence the transformed phenotype in human mammary epithelial cells. (Cancer Res 2006; 66(24): 11632-43)

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Section: Discussionmentioning

confidence: 85%

Multiple Interacting Oncogenes on the 8p11-p12 Amplicon in Human Breast Cancer

Yang¹,

Streicher²,

et al. 2006

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“…Chibby (Cby), a small (126 aa) protein antagonizes Wnt/ -catenin signaling by forming a ternary complex with protein 14-3-3 andcatenin [418,419]. The protein TC-1, associated with thyroid cancer, in turn can bind to Cby and inhibit its interactions withcatenin, leading to an upregulation of -catenin target genes [420,421]. Further tissue-specific proteins like Osterix (osteoblastsspecific transcription factor) are also able to repress the transcriptional complex through a disruption of Tcf binding to DNA [422].…”

Section: The -Catenin Tcf/lef Transcription Complexmentioning

confidence: 99%

Wnt/beta-Catenin Signaling and Small Molecule Inhibitors

Voronkov¹,

Krauß²

2012

CPD

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Wnt/ -catenin signaling is a branch of a functional network that dates back to the first metazoans and it is involved in a broad range of biological systems including stem cells, embryonic development and adult organs. Deregulation of components involved in Wnt/ -catenin signaling has been implicated in a wide spectrum of diseases including a number of cancers and degenerative diseases. The key mediator of Wnt signaling, -catenin, serves several cellular functions. It functions in a dynamic mode at multiple cellular locations, including the plasma membrane, where -catenin contributes to the stabilization of intercellular adhesive complexes, the cytoplasm where -catenin levels are regulated and the nucleus where -catenin is involved in transcriptional regulation and chromatin interactions. Central effectors of -catenin levels are a family of cysteine-rich secreted glycoproteins, known as Wnt morphogens. Through the LRP5/6-Frizzled receptor complex, Wnts regulate the location and activity of the destruction complex and consequently intracellularcatenin levels. However, -catenin levels and their effects on transcriptional programs are also influenced by multiple other factors including hypoxia, inflammation, hepatocyte growth factor-mediated signaling, and the cell adhesion molecule E-cadherin. The broad implications of Wnt/ -catenin signaling in development, in the adult body and in disease render the pathway a prime target for pharmacological research and development. The intricate regulation of -catenin at its various locations provides alternative points for therapeutic interventions.

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“…An extensive karyotype description has been reported only for the FTC133 and WRO82-1 cell lines (12,21,28). In particular, the FTC133 cells revealed significant gains in part or whole of chromosomes 1,11,6,7,8,14,15,19, and 20, and losses in chromosomes 16, 21, and 22 (28). The hyperdiploid karyograms in the FTC133 and WRO82-1 cells (62-71 and 68-77 chromosomes, respectively) have also been reported (12).…”

Section: Ftcmentioning

confidence: 99%

“…Molecular technologies such as microarrays, serial analysis of gene expression, and proteomics have shown promising results that may allow a more definitive diagnosis and proper molecular classification of thyroid cancers. In this regard, microarrays have been successfully used to identify prognostic markers that offer the possibility of tailoring better treatment regimens for thyroid cancer (4)(5)(6)(7)(8)(9). Because of the heterogeneous nature of thyroid cancers it is imperative that appropriate experimental systems be used to delineate the underlying molecular mechanisms of tumorigenesis.…”

Section: Introductionmentioning

confidence: 99%