DNA methylation-mediated down-regulation of TMEM130 promotes cell migration in breast cancer

Breast cancer is the most common female cancer worldwide. DNA methylation is a common modification in epigenetics and affects the prognosis of breast cancer by changing gene expression. In the present study, we aim to investigate the role of DNA methylation in TMEM130 gene expression, and the functi...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Acta histochemica 2021-12, Vol.123 (8), p.151814-151814, Article 151814
Hauptverfasser: Liu, Hong, Xie, Hong-qiang, Zhao, Yan, Zhang, Wen, Zhang, Yan
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Breast cancer is the most common female cancer worldwide. DNA methylation is a common modification in epigenetics and affects the prognosis of breast cancer by changing gene expression. In the present study, we aim to investigate the role of DNA methylation in TMEM130 gene expression, and the function of TMEM130 in breast cancer cell migration. The transcriptional expression of TMEM130 was detected by qRT-PCR in breast cancer cell lines and tissues. Bisulfite sequencing PCR (BSP) was used to confirm the methylation status of TMEM130 promoter. Then, TMEM130 was transfected in breast cancer cell lines and to explore its role in cell migration by Transwell and western blot. TMEM130 mRNA expression was decreased in breast cancer cell lines and tissues, and consistent with the data in The Cancer Genome Atlas (TCGA). The promoter of TMEM130 was hypermethylated in breast cancer and the expression of TMEM130 could be restored by the methyltransferase inhibitor. Overexpression of TMEM130 could inhibit cell migration ability in breast cancer cell lines. Taken together, these results indicate TMEM130 downregulation and hypermethylation might contribute to breast cancer migration and TMEM130 might be a promising biomarker for breast cancer.
ISSN:0065-1281
1618-0372
DOI:10.1016/j.acthis.2021.151814