Dokumentdetails
ID

doi:10.1038/s41419-024-06451-w...

Autor
Gui, Yanping Qian, Xiaoping Ding, Youxiang Chen, Qianqian Fangyu Ye Ye, Yuting Hou, Yingjian Yu, Jun Zhao, Li
Langue
en
Editor

Nature

Kategorie

Life Sciences

Jahr

2024

Auflistungsdatum

24.01.2024

Schlüsselwörter
stemness phosphorylation nanog cancer c-fos colon
Metrisch

Zusammenfassung

Acquired drug resistance is one of the most common limitations for the clinical response of colon cancer to 5-Fluorouracil (5-FU)-based chemotherapy.

The relevant molecular mechanisms might be diversity, but still not be elucidated clearly.

In this study, we aimed to investigate the potential mechanisms of c-Fos, a subfamily of activator protein-1, in 5-FU chemoresistance.

We determined that phosphorylated c-Fos promoted colon cancer cells resistance to 5-FU by facilitating the cancer stemness.

Mechanically, 5-FU treatment induced autolysosome-dependent degradation of TMPO, which subsequently triggered ERK-mediated phosphorylation of c-Fos.

Additionally, c-Fos was found to bind to the promoter of NANOG and phosphorylation of c-Fos at Ser 374 was required for its regulation of NANOG expression.

NANOG ablation impaired c-Fos/p-c-Fos induced 5-FU resistance and stemness.

Taken together, these findings revealed that TMPO-mediated phosphorylation of c-Fos conferred 5-FU resistance by regulating NANOG expression and promoting cell stemness in colon cancer cells.

c-Fos could be as a therapeutic target for colon cancer.

Gui, Yanping,Qian, Xiaoping,Ding, Youxiang,Chen, Qianqian,Fangyu Ye,Ye, Yuting,Hou, Yingjian,Yu, Jun,Zhao, Li, 2024, c-Fos regulated by TMPO/ERK axis promotes 5-FU resistance via inducing NANOG transcription in colon cancer, Nature

Dokumentieren

Öffnen

Teilen

Quelle

Artikel empfohlen von ES/IODE AI