SENP2通过SETDB1去SUMO化和增强脂肪酸代谢促进食管鳞癌增殖。

Sun Linyi, Ma Ke, Zhang Shaoyuan, Gu Jianmin, Wang Hao, Tan Lijie

Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.

Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.

Heliyon. 2024 Jul 2;10(13):e34010. doi: 10.1016/j.heliyon.2024.e34010. eCollection 2024 Jul 15.

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 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.

食管鳞状细胞癌（ESCC）预后较差，其代谢重编程机制尚不清楚。小泛素样修饰物（SUMO）特异性蛋白酶（SENP2）在一些正常组织中与脂肪酸代谢高度相关。因此，本研究探讨SENP2与ESCC之间的相关性及可能机制。与正常组织相比，ESCC组织中SENP2表达上调，高水平与总体生存率低相关。敲低SENP2可抑制ESCC增殖、脂肪酸摄取和氧化。RNA测序表明，SENP2通过去SETDB1的SUMO化上调PPARγ、CPT1A、ACSL1和CD36。SENP2促进ESCC增殖并增强脂肪酸摄取和氧化。SENP2高表达可能是ESCC患者预后不良的生物标志物。