Evidence map›Paper›PMID 32072403›Full record

ArticleMolecular biology reports2020

Investigation of promoter methylation of FSCN1 gene and FSCN1 protein expression in differentiated thyroid carcinomas.

Mojdeh Mahdiannasser, Vahid Haghpanah, Elia Damavandi, Majid Kabuli, Seyed Mohammad Tavangar, Bagher Larijani, Mohsen Ghadami

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Article in Molecular biology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 41% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 6 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Mojdeh MahdiannasserDepartment of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Poursina St, Tehran, Iran.ORCID http://orcid.org/0000-0002-6526-8222
Vahid HaghpanahEndocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Poursina St, District 6, Tehran, Tehran Province, Iran.
Elia DamavandiSpecialized Medical Genetic Center (SMGC) of ACECR, 4th floor, No 65, Aboureihan St, Enghelab Ave., Tehran, Iran.ORCID http://orcid.org/0000-0003-4501-0643
Majid KabuliDepartment of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Poursina St, Tehran, Iran.
Seyed Mohammad TavangarDepartment of Pathology, Dr. Shariati Hospital, Tehran University of Medical Sciences, Jalal Al Ahmad Junction, Karegar Shomali St, Tehran, Iran.ORCID http://orcid.org/0000-0002-4253-2385
Bagher LarijaniEndocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Poursina St, District 6, Tehran, Tehran Province, Iran.
Mohsen GhadamiDepartment of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Poursina St, Tehran, Iran. mghadami@tums.ac.ir.ORCID http://orcid.org/0000-0002-7404-727X
Tehran University of Medical Sciences · IRAcademic Center for Education, Culture and Research · IRShariati Hospital · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FSCN1 gene encodes an actin-bundling protein, FSCN1, which is involved in formation of actin-based structures that contribute to cell migration. High levels of FSCN1 expression is observed in cells with extended membranes and protrusions. Moreover, up-regulation of FSCN1 has been reported in several epithelial carcinomas. Therefore, FSCN1 is thought to play a role in cell movement and invasion. However, the mechanism behind FSCN1 up-regulation is not known. We investigated the expression of FSCN1 using immunohistochemistry. Methylation-specific PCR was adopted to analyze the methylation status of FSCN1 promoter as a potential regulatory mechanism in FSCN1 expression. The samples included papillary thyroid carcinoma, follicular thyroid carcinoma and goiter samples (controls). Methylation of FSCN1 promoter was observed in 50% of follicular, 48.6% of papillary and 60% of controls. The promoter was unmethylated in 16.7% of follicular samples, 5.7% of papillary samples and 26.7% of controls. In the remaining 33.3% of follicular and 45.7% of papillary samples as well as 13.3% of controls, both methylated and unmethylated alleles were amplified, a condition referred to as semi-methylation. The results showed that FSCN1 promoter was significantly hypomethylated in papillary cases while the methylation status was not significantly altered in follicular cases. On the other hand, FSCN1 was expressed in only nine papillary samples. Regarding protein expression and methylation status, we suggest that hypomethylation of FSCN1 promoter in papillary thyroid carcinoma does not lead to overexpression of FSCN1 and that there might be other regulatory mechanisms involved in FSCN1 up-regulation.

Indexed as

DNA MethylationGene Expression Regulation, NeoplasticPromoter Regions, GeneticBiomarkers, TumorCarrier ProteinsCell Line, TumorCpG IslandsFemaleHumansImmunohistochemistryMaleMicrofilament ProteinsNeoplasm GradingThyroid NeoplasmsBiomarkers, TumorCarrier ProteinsFSCN1 protein, humanMicrofilament ProteinsFSCN1ImmunohistochemistryMethylationPromoterThyroid cancer

Identifiers

PMID32072403
OpenAlexW3008279669

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.