SENP2 promotes ESCC proliferation through SETDB1 deSUMOylation and enhanced fatty acid metabolism.
Heliyon
; 10(13): e34010, 2024 Jul 15.
Article
en En
| MEDLINE
| ID: mdl-39071660
ABSTRACT
Esophageal squamous cell carcinoma (ESCC) has a poor prognosis, and its metabolic reprogramming mechanism remains unclear. Small ubiquitin-like modifier(SUMO) -specific protease(SENP2) is highly related to fatty acids metabolism in some normal tissue. Thus, this study investigates the correlation between SENP2 and ESCC, and the possible mechanism. SENP2 expression was up-regulated in ESCC tissues compared to normal tissues, with high levels associated with poor overall survival rates. Knockdown of SENP2 inhibited ESCC proliferation, fatty acid uptake, and oxidation in vitro. RNA-seq indicated that SENP2 upregulated PPARγ, CPT1A, ACSL1, and CD36, through the deSUMOylation of SETDB1. SENP2 promotes ESCC proliferation and enhances fatty acid uptake and oxidation. High expression of SENP2 may be a poor prognostic biomarker for ESCC patients.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Idioma:
En
Revista:
Heliyon
Año:
2024
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Reino Unido