Literature DB >> 29300379

The role of SMAD3 in the genetic predisposition to papillary thyroid carcinoma.

Yanqiang Wang1, Huiling He1, Sandya Liyanarachchi1, Luke K Genutis1, Wei Li1, Lianbo Yu2,3, John E Phay4, Rulong Shen5, Pamela Brock6, Albert de la Chapelle7.   

Abstract

PURPOSE: To identify and characterize the functional variants, regulatory gene networks, and potential binding targets of SMAD3 in the 15q22 thyroid cancer risk locus.
METHODS: We performed linkage disequilibrium (LD) and haplotype analyses to fine map the 15q22 locus. Luciferase reporter assays were applied to evaluate the regulatory effects of the candidate variants. Knockdown by small interfering RNA, microarray analysis, chromatin immunoprecipitation (ChIP) and quantitative real-time polymerase chain reaction assays were performed to reveal the regulatory gene network and identify its binding targets.
RESULTS: We report a 25.6-kb haplotype within SMAD3 containing numerous single-nucleotide polymorphisms (SNPs) in high LD. SNPs rs17293632 and rs4562997 were identified as functional variants of SMAD3 by luciferase assays within the LD region. These variants regulate SMAD3 transcription in an allele-specific manner through enhancer elements in introns of SMAD3. Knockdown of SMAD3 in thyroid cancer cell lines revealed its regulatory gene network including two upregulated genes, SPRY4 and SPRY4-IT1. Sequence analysis and ChIP assays validated the actual binding of SMAD3 protein to multiple SMAD binding element sites in the region upstream of SPRY4.
CONCLUSION: Our data provide a functional annotation of the 15q22 thyroid cancer risk locus.

Entities:  

Keywords:  15q22 locus; SMAD3; downstream targets; functional variants; papillary thyroid carcinoma

Mesh:

Substances:

Year:  2018        PMID: 29300379      PMCID: PMC6030507          DOI: 10.1038/gim.2017.224

Source DB:  PubMed          Journal:  Genet Med        ISSN: 1098-3600            Impact factor:   8.822


  39 in total

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