Article
Immunology
Hongwei Wang, Xu Wang, Yubin Shen, Yanmin Wang, Tianyun Yang, Jinyuan Sun, Song Liu
Summary: Chronic intermittent hypoxia (CIH) is a characteristic pathological change of obstructive sleep apnea syndrome (OSAS). Inflammation of microglia induced by CIH plays a crucial role in OSAS-associated cognitive dysfunction. SUMO-specific proteases 1 (SENP1) has been implicated in tumor inflammatory microenvironment and cell migration, but its role in CIH-induced neuroinflammation is still unknown.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2023)
Article
Cell Biology
Hongwei Wang, Tianyun Yang, Jinyuan Sun, Sisen Zhang, Song Liu
Summary: The study found that SENP1 regulates neuroinflammation induced by IH by modulating the SUMOylation of NEMO, activating the NF-kappa B pathway and affecting cognition. Targeting SENP1 may represent a novel therapeutic strategy for IH-induced cognitive decline.
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
(2021)
Article
Cell Biology
Hongwei Wang, Wei Xiong, Sitong Hang, Yanmin Wang, Sisen Zhang, Song Liu
Summary: This study investigated the precise mechanism underlying cognitive decline after IH insult, revealing that SENP1 downregulation could exacerbate inflammation and neuronal apoptosis, further reducing the level of PPARγ. However, the application of PPARγ agonist could suppress the enhancement of inflammation and neuronal apoptosis. Behavioral experiments in IH mice showed that SENP1 downregulation worsened cognitive impairment.
Article
Oncology
Min Wei, Xinping Huang, Liming Liao, Yonglu Tian, Xiaofeng Zheng
Summary: The SUMOylation-induced LLPS of RNF168 suppresses the DNA damage response, while SENP1 decreases RNF168 SUMOylation to promote DNA damage repair and cancer cell resistance.
Article
Cell Biology
Kan Yang, Yuhan Shi, Xiujuan Du, Jincheng Wang, Yuefang Zhang, Shifang Shan, Yiting Yuan, Ruoqing Wang, Chenhuan Zhou, Yuting Liu, Zilin Cai, Yanzhi Wang, Liu Fan, Huatai Xu, Juehua Yu, Jinke Cheng, Fei Li, Zilong Qiu
Summary: Autism spectrum disorder (ASD) is highly heritable and can lead to social interaction defects and repetitive behaviors. A study found a de novo heterozygous gene-truncating mutation in the Sentrin-specific peptidase (SENP1) gene in individuals with ASD without neurodevelopmental delay. This mutation causes autistic-like symptoms in Senp1(+/-) mice, with affected synaptic functions in the retrosplenial agranular (RSA) cortex. Reintroducing SENP1 or FMRP in RSA can fully rescue synaptic function defects and autistic-like symptoms in Senp1(+/-) mice.
Article
Biochemistry & Molecular Biology
Kezhou Wang, Jie Xiong, Yiwen Lu, Lifeng Wang, Tian Tian
Summary: Macrophages are crucial immune cells in tumour immunity, and the subtypes of macrophages, M1 and M2, play different roles in response to different microenvironments. The transcription factor KLF4 and its SUMOylation have been shown to regulate macrophage polarization. SENP1, a specific protease for KLF4 de-SUMOylation, is found to affect M1 macrophage polarization and the activity of tumour cells. This suggests that the SENP1-KLF4 axis could be a potential target in cancer therapy.
Article
Biochemistry & Molecular Biology
Krishna M. Chauhan, Yingxiao Chen, Yiyi Chen, Andrew T. Liu, Xiao-Xin Sun, Mu-Shui Dai
Summary: The study reveals that SENP1 is a critical p53 deSUMOylating enzyme, and its depletion induces p53 transactivation activity and synergizes with DNA damage-inducing agent etoposide to activate p53 and inhibit cancer cell growth.
JOURNAL OF CELLULAR BIOCHEMISTRY
(2021)
Article
Oncology
Xin Liu, Shenglin Zhang, Yi Dong, Yunpeng Xie, Qingshan Li
Summary: Gliomas, the most common primary brain tumors in adults, present clinical challenges due to their infiltrative growth patterns and high relapse tendencies. This study identified SENP1 as an upregulated SUMOylation regulator in gliomas and demonstrated its association with poor prognoses. Mechanistically, SENP1 inhibited SIRT1 expression through de-SUMOylation, leading to the activation of NF-kappa B and promotion of glioma cell malignant phenotype. This suggests that SENP1-mediated de-SUMOylation of SIRT1 could have therapeutic implications for gliomas.
EXPERIMENTAL CELL RESEARCH
(2023)
Article
Chemistry, Medicinal
Mao-xu Ge, Wei-xiao Niu, Yun-yang Bao, Zhen-ning Lu, Hong-wei He
Summary: This study aimed to evaluate the antifibrotic activity of sclareol (SCL) from Salvia sclarea on liver fibrosis and explore its underlying mechanisms. The results showed that SCL treatment inhibited the profibrotic tendency of activated hepatic stellate cells. In animal models, SCL administration reduced liver injury and collagen accumulation. Mechanistic studies revealed that SCL mediated VEGFR2 SUMOylation, resulting in the inhibition of the interaction between VEGFR2 and STAT3 and the suppression of downstream STAT3 phosphorylation.
PHYTOTHERAPY RESEARCH
(2023)
Article
Cell Biology
Yali Zhang, Yanni Ma, Guixian Wu, Mingling Xie, Chengxin Luo, Xiangtao Huang, Feng Tian, Jieping Chen, Xi Li
Summary: Mantle cell lymphoma (MCL) is a highly aggressive lymphoma, and the upregulation of SENP1 in MCL patients has been found to inhibit tumor cell proliferation and promote apoptosis. Additionally, the downregulation of SENP1 affects the JAK-STAT5 pathway and upregulates SOCS2, leading to suppressed MCL tumor growth in vivo, suggesting SENP1 as a potential therapeutic target for MCL.
CELL DEATH DISCOVERY
(2021)
Article
Cell Biology
Jun Zhang, Guo-lin Tan, Ming Jiang, Tian-sheng Wang, Guo-hui Liu, Shan-shan Xiong, Xiang Qing
Summary: This study investigated the effect of SUMO modification of STAT1 protein on the proliferation and invasion of nasopharyngeal carcinoma (NPC). The analysis of gene expression profiles revealed differentially expressed genes in NPC. Further analysis identified the high expression of SENP1 and SENP2 to be closely related to poor prognosis in NPC. Experimental results confirmed that SENP1 promoted the proliferation and invasion of NPC through inhibiting the SUMOylation of STAT1.
CELLULAR SIGNALLING
(2023)
Article
Biochemistry & Molecular Biology
Ming-Cheng Chen, Do Chi Nhan, Chiung-Hung Hsu, Tso-Fu Wang, Chi-Cheng Li, Tsung-Jung Ho, B. Mahalakshmi, Mei-Chih Chen, Liang-Yo Yang, Chih-Yang Huang
Summary: This study found that the accumulation of SENP1 and HIF-1α proteins in irinotecan-resistant colorectal cancer cells promoted drug resistance and poor clinical outcomes. Silencing the SENP1 gene reduced cell migration ability and restored sensitivity to irinotecan treatment.
JOURNAL OF CELLULAR BIOCHEMISTRY
(2021)
Article
Biochemistry & Molecular Biology
Heng Cai, Xiyun Bian, Liangyu Chen, Nan Zhang, Lili Li, Wei Tang, Xiaozhi Liu, Zhiqing Li
Summary: The study shows that SI-AC can protect against cerebral I/R injury by inhibiting oxidative stress and mitochondrial dysfunction through regulation of Sirt3 deSUMOylation, providing a promising therapeutic approach for acute cerebral I/R injury treatment.
FREE RADICAL BIOLOGY AND MEDICINE
(2021)
Article
Endocrinology & Metabolism
Haopeng Lin, Nancy Smith, Aliya F. Spigelman, Kunimasa Suzuki, Mourad Ferdaoussi, Tamadher A. Alghamdi, Sophie L. Lewandowski, Yaxing Jin, Austin Bautista, Ying Wayne Wang, Jocelyn E. Manning Fox, Matthew J. Merrins, Jean Buteau, Patrick E. MacDonald
Summary: The deSUMOylating enzyme SENP1 plays a critical role in regulating pancreatic islet function following high-fat diet, modulating glucose tolerance through insulin secretion downstream of incretin signaling.
Article
Biochemistry & Molecular Biology
Dong-Dong Chen, Qi Shi, Xin Liu, Dong-Lin Liang, Yue-Zhang Wu, Qin Fan, Kang Xiao, Cao Chen, Xiao-Ping Dong
Summary: Post-translational modifications of proteins, such as acetylation and SUMOylation, are crucial in regulating protein functions and pathophysiology of diseases, including neurodegenerative diseases. This study demonstrates that prion infection leads to abnormal acetylation profiles and reduced deacetylases, along with increased levels of SUMO1 modifications. The dysregulation of the SENP1-SUMO1-Sirt pathway induced by prions or Cyto-PrP accumulation triggers aberrant mitochondrial deacetylation and respiratory chain dysfunction.
ACS CHEMICAL NEUROSCIENCE
(2023)