ArticlePloS one2025
Hypotaurine promotes glioma cell invasion by hypermethylating the Wnt5a promoter.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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1 citing paper in PubMed.
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5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Glioma is a particularly lethal central nervous system tumor. Identifying the boundary between gliomas and normal tissues is difficult due to their infiltrative and invasive growth characteristics. This can result in the inevitable recurrence of the tumor after surgery. Preventing the residual tumor from growing or spreading is a major obstacle in treating gliomas. An earlier study suggested that hypotaurine could enhance the invasion of glioma cells while inhibiting the activity of demethylases. The hypotaurine synthesis-deficient U251 cell line usage showed a decrease in the cells' invasion capability. Analysis of gene expression profiles showed that reducing the activity of a critical enzyme in hypotaurine production, 2-aminoethanethiol dioxygenase (ADO), had a notable effect on the extracellular matrix-receptor interaction. Decreased intracellular ADO expression led to a significant increase in Wnt5a expression. Cells exposed to hypotaurine exhibited decreased levels of both intracellular Wnt5a protein and its corresponding mRNA. The observed characteristic was linked to increased methylation of the Wnt5a gene promoter, possibly due to hypotaurine's ability to inhibit demethylase enzymes. To sum up, the research showed that U251 cells lacking hypotaurine synthesis were susceptible to epigenetic changes, and Wnt5a seemed to function as a cancer inhibitor in this scenario. It would be beneficial to reevaluate this tumor suppressive effect in real tumor samples, which may contribute to the development of new glioma interference strategies.
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