ArticleOncotarget2016
Transcriptional regulation of the potential tumor suppressor ABI3 gene in thyroid carcinomas: interplay between methylation and NKX2-1 availability.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Reduced expression ofFrontiers in endocrinology · 2024Article
- Article
- Epigenetic Modifications in Thyroid Cancer Cells Restore NIS and Radio-Iodine Uptake and Promote Cell Death.Journal of clinical medicine · 2018Article
- Microglia express ABI3 in the brains of Alzheimer's disease and Nasu-Hakola disease.Intractable & rare diseases research · 2017Article
- ABI3, a component of the WAVE2 complex, is potentially regulated by PI3K/AKT pathway.Oncotarget · 2017Article
- Epigenetic Modifications: Novel Therapeutic Approach for Thyroid Cancer.Endocrinology and metabolism (Seoul, Korea) · 2017Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported that ABI3 expression was decreased in thyroid cancer tissues and that ectopic expression of ABI3 in a follicular thyroid carcinoma cell line delayed cell cycle progression and inhibited cell proliferation, invasion, migration and tumor formation in athymic mice. These data indicated that ABI3 is a tumor suppressor gene; however the mechanism through which ABI3 is silenced in thyroid carcinomas is unknown. We here show that treatment of four follicular thyroid carcinoma cell lines with 5-aza-dC induced demethylation of a specific region of the ABI3 promoter and restored ABI3 expression. In contrast, 5-aza-dC treatment did not restore ABI3 expression in a non-thyroid cell line, suggesting a tissue-specific regulation. We additionally show that 8 CpG sites located within the ABI3 promoter are hypermethylated in most thyroid carcinoma samples and the degree of methylation correlated with ABI3 expression. Narrowing the region to specific CpG sites, the CpG4-6 sites showed the largest difference between benign and malignant lesions. In silico analysis revealed that these CpG sites flank a canonical binding site for NKX2-1, a thyroid specific transcriptional factor. Analysis of thyroid samples shows a correlation between NKX2-1 and ABI3 expression. In vitro assays demonstrate that NKX2-1 was required for ABI3 expression. Luciferase assay further confirmed the promoter activity of this region, which was increased when the cells were co-transfected with NKX2-1. Our study shows that the transcriptional silencing of ABI3 in cancer cells occurs via methylation and uncovered a previously unrecognized role for NKX2-1 in the regulation of ABI3.
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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.