Epigenetic regulation of human WIF1 and DNA methylation situation of WIF1 and GSTM5 in urothelial carcinoma

May 19, 2023Heliyon

Epigenetic control and DNA methylation of WIF1 and GSTM5 genes in bladder cancer

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Circadian Biology on OpenScience ↗PubMed ↗DOI ↗

Abstract

A positive relationship exists between WIF1 mRNA expression and the survival probability of bladder cancer patients.

WIF1 gene expression could be enhanced by the DNA demethylation drug 5-aza-2'-deoxycytidine and the histone deacetylase inhibitor trichostatin A.
Overexpression of WIF1 inhibited cell proliferation and migration in bladder cancer cells, supporting its role as a tumor suppressor.
5-Aza-dC increased WIF1 gene expression in a dose-dependent manner while reducing DNA methylation levels.
Analysis showed no difference in DNA methylation levels of the WIF1 promoter region -184 to +29 between bladder cancer patients and controls.
A higher level of GSTM5 DNA methylation was confirmed in bladder cancer patients compared to controls.
The WIF1 promoter region -258 to -89 is suggested as a useful area for DNA methylation assays in bladder cancer.

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WNT inhibitory factor 1 () is known to function as a tumor suppressor gene; it inhibits oncogene activation by preventing WNT signaling. This study investigated the epigenetic regulation of WIF1 gene in bladder cancer. We observed a positive relationship between WIF1 mRNA expression and survival probability of bladder cancer patients. The WIF1 gene expression could be enhanced by DNA demethylation drug 5-aza-2'-deoxycytidine (5-aza-dC) and histone deacetylase inhibitor trichostatin A (TSA), suggesting that epigenetic modifications could regulate WIF1 gene expression. Overexpression of WIF1 inhibited cell proliferation and migration in 5637 cells, confirming the tumor suppressor role of WIF1. 5-Aza-dC dose dependently increased WIF1 gene expression while reducing DNA methylation level, suggesting that reversing WIF1 DNA methylation could activate its gene expression. We collected the cancer tissues and urine pellets of bladder cancer patients and only urine pellets from non-bladder cancer volunteers for DNA methylation analysis, but the methylation level ofgene -184 to +29 did not differ between patients and controls. We also analyzed glutathione-transferase Mu 5 (GSTM5) gene methylation level because GSTM5 DNA hypermethylation was suggested to be a tumor biomarker in our previous study. It confirmed a higher GSTM5 DNA methylation in bladder cancer patients than in controls. In summary, this study suggests that the 5-aza-dC activated WIF1 gene which showed an anti-cancer effect, whilepromoter -184 to +29 did not provide a suitable methylation assay region in clinical samples. In contrast,promoter -258 to -89 is a useful region for DNA methylation assay because it shows a higher methylation level in bladder cancer patients. WIF1WIF1S WIF1GSTM5

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Epigenetic regulation of human WIF1 and DNA methylation situation of WIF1 and GSTM5 in urothelial carcinoma

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