SENP2 promotes ESCC proliferation through SETDB1 deSUMOylation and enhanced fatty acid metabolism
Linyi Sun, MSc,
Ke Ma, MD,
Shaoyuan Zhang, MD,
Jianmin Gu, MD,
Hao Wang, MD,
Lijie Tan, MD
Affiliations
Linyi Sun, MSc
Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China; Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China
Ke Ma, MD
Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China; Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China
Shaoyuan Zhang, MD
Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China; Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China
Jianmin Gu, MD
Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China; Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China
Hao Wang, MD
Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China; Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China; Corresponding author. Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Cancer Center, Zhongshan Hospital, Fudan University, No 180, Fenglin Rd, Xuhui District, Shanghai, 200032, China.
Lijie Tan, MD
Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China; Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China; Corresponding author. Department of Thoracic Surgery, Zhongshan Hospital, Fudan University Cancer Center, Zhongshan Hospital, Fudan University No 180, Fenglin Rd, Xuhui District, Shanghai, 200032, China.
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.
