YTHDC1 inhibits cell proliferation and angiogenesis in cervical cancer by regulating m6A modification of SOCS4 mRNA

Background Cervical cancer (CC) is one of the most common tumors in women, with a high mortality rate. YTHDC1 has been discovered to be involved in the progression of several cancers by acting as a tumor suppressor. However, the detailed regulatory role of YTHDC1 in CC remains unclear. Our study aim...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Molecular & cellular toxicology 2024, 20(3), , pp.533-540
Hauptverfasser: Chen, Sihe, Chen, Yongheng, Yu, Lanting, Hu, Xiangmei
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Background Cervical cancer (CC) is one of the most common tumors in women, with a high mortality rate. YTHDC1 has been discovered to be involved in the progression of several cancers by acting as a tumor suppressor. However, the detailed regulatory role of YTHDC1 in CC remains unclear. Our study aimed to investigate the effects of YTHDC1 on CC progression. Objectives To investigate the regulatory functions of YTHDC1 in CC. Results First, through TCGA database, YTHDC1 expression was found to be down-regulated in CC. In addition, the expression of YTHDC1 was also decreased in CC tissues and cells. Moreover, our results showed that YTHDC1 repressed cell proliferation and facilitated cell apoptosis. Additionally, YTHDC1 inhibited angiogenesis and metastasis. Further investigations revealed that YTHDC1 accelerated SOCS4 m6A modification to enhance SOCS4 expression. Finally, we identified that the suppressive effects mediated by YTHDC1 on CC progression were reversed by silencing SOCS4. Conclusion Our study for the first time showed that YTHDC1 inhibited cell proliferation and angiogenesis of cervical cancer by regulating m6A modification of SOCS4 mRNA. This finding may provide a potential therapeutic molecular target for CC.
ISSN:1738-642X
2092-8467
DOI:10.1007/s13273-023-00360-3