Measurement of &lt;i&gt;TFF3&lt;/i&gt; mRNA in aspirates from thyroid nodules using mesh filtration: The first clinical trial in 130 cases

Yamada, Hiroya; Takano, Toru; Kihara, Minoru; Hirokawa, Mitsuyoshi; Yoshida, Hiroshi; Watanabe, Mikio; Iwatani, Yoshinori; Hidaka, Yoh; Miyauchi, Akira

doi:10.1507/endocrj.ej12-0077

Cited by 4 publications

(2 citation statements)

References 30 publications

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“…The hTFF3 cDNA is 222 bp in length (GenBank accession No. NM003226.3) and it encodes 73 amino acids, including 14 that encode forward signal peptide and 59 backward mature amino acids [9], [10]. A variety of substances have been found to regulate the expression of hTFF3, and its corresponding response elements, such as estrogen, upstream stimulatory factor (USF), interleukins, and hypoxia-inducible factor 1 (HIF-1), etc [11].…”

Section: Resultsmentioning

confidence: 99%

Cloning and Characterization of the Human Trefoil Factor 3 Gene Promoter

et al. 2014

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Human trefoil factor 3 (hTFF3) is a small-molecule peptide with potential medicinal value. Its main pharmacological function is to alleviate gastrointestinal mucosal injuries caused by various factors and promote the repair of damaged mucosa. However, how its transcription is regulated is not yet known. The aim of this study was to clone the hTFF3 gene promoter region, identify the core promoter and any transcription factors that bind to the promoter, and begin to clarify the regulation of its expression. The 5′ flanking sequence of the hTFF3 gene was cloned from human whole blood genomic DNA by PCR. Truncated promoter fragments with different were cloned and inserted into the pGL3-Basic vector to determine the position of the core hTFF3 promoter. Transcription element maintaining basic transcriptional activity was assessed by mutation techniques. Protein-DNA interactions were analyzed by chromatin immunoprecipitation (ChIP). RNA interference and gene over-expression were performed to assay the effect of transcription factor on the hTFF3 expression. The results showed that approximately 1,826 bp of the fragment upstream of hTFF3 was successfully amplified, and its core promoter region was determined to be from −300 bp to −280 bp through analysis of truncated mutants. Mutation analysis confirmed that the sequence required to maintain basic transcriptional activity was accurately positioned from −300 bp to −296 bp. Bioinformatic analysis indicated that this area contained a Sp1 binding site. Sp1 binding to the hTFF3 promoter was confirmed by ChIP experiments. Sp1 over-expression and interference experiments showed that Sp1 enhanced the transcriptional activity of the hTFF3 promoter and increased hTFF3 expression. This study demonstrated that Sp1 plays an important role in maintaining the transcription of hTFF3.

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Section: Resultsmentioning

confidence: 99%

Cloning and Characterization of the Human Trefoil Factor 3 Gene Promoter

et al. 2014

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“…Decreased expression of TFF3 mRNA in thyroid follicular carcinoma was first reported by Takano T et al [22] and this finding was subsequently reproduced by several groups in follicular, papillary and anaplastic carcinomas [23][24][25][26] and validated at protein level by an immunohistochemical study [27]. TFF3 mRNA is one of the most promising biomarkers for pre-operative diagnosis of thyroid cancer and the development of a biomarker assay based on the measuring of TFF3 mRNA level in thyroid aspirates is ongoing [28]. However, to the best of our knowledge, the functional role of TFF3 in the development of thyroid cancer has not been elucidated so far.…”

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confidence: 83%

Trefoil factor 3 is required for differentiation of thyroid follicular cells and acts as a context-dependent tumor suppressor

Ābols¹,

Ducena²,

Andrējeva³

et al. 2015

neo

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Trefoil factor 3 (TFF3) is overexpressed in a variety of solid epithelial cancers, where it has been shown to promote migration, invasion, proliferation, survival and angiogenesis. On the contrary, in the majority of thyroid tumors, it is downregulated, yet its role in the development of thyroid cancer remains unknown. Here we show that TFF3 exhibits strong cytoplasmic staining of normal thyroid follicular cells and colloid and the staining is increased in hyperfunctioning thyroid nodules, while it is decreased in all thyroid cancers of follicular cell origin. By meta-analysis of gene expression datasets, we found that in the thyroid cancer, conversely to the breast cancer, the expression of TFF3 mRNA was downregulated by estrogen signaling and confirmed this by treating thyroid cancer cells with estradiol. Forced expression of TFF3 in anaplastic thyroid cancer cells resulted in decreased cell proliferation, clonal spheroid formation and entry into the S phase. Furthermore, it induced acquisition of epithelial-like cell morphology and expression of the differentiation markers of thyroid follicular cells and transcription factors implicated in the thyroid morphogenesis and function. Taken together, this study provides the first evidence that TFF3 may act as a tumor suppressor or an oncogene depending on the cellular context.

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Pitfalls in Molecular-Based Diagnosis Using Thyroid Aspirates

Takano

2019

Thyroid FNA Cytology

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Measurement of <i>TFF3</i> mRNA in aspirates from thyroid nodules using mesh filtration: The first clinical trial in 130 cases

Cited by 4 publications

References 30 publications

Cloning and Characterization of the Human Trefoil Factor 3 Gene Promoter

Cloning and Characterization of the Human Trefoil Factor 3 Gene Promoter

Trefoil factor 3 is required for differentiation of thyroid follicular cells and acts as a context-dependent tumor suppressor

Pitfalls in Molecular-Based Diagnosis Using Thyroid Aspirates

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