Extracellular vesicles-transferred SBSN drives glioma aggressiveness by activating NF-κB via ANXA1-dependent ubiquitination of NEMO
Chen，Han1,2; Chen，Xuhong2,3; Zhang，Zhuojun1,2; Bao，Wenhao1,2; Gao，Zhiqing1,2; Li，Difeng1,2; Xie，Xiaoyi1,2; Zhou，Ping1,2; Yang，Chunxiao1,2; Zhou，Zhongqiu4; Pan，Jinyuan5; Kuang，Xiangqin1,2; Tang，Ruiming6; Feng，Zhengfu6; Zhou，Lihuan6; Zhu，Dachun7; Yang，Jianan1,8; Wang，Lan9; Huang，Hongbiao1,2; Tang，Daolin10; Liu，Jinbao1,2; Jiang，Lili1,2
|Corresponding Author||Liu，Jinbao; Jiang，Lili|
Glioma is the most common malignant primary brain tumor with aggressiveness and poor prognosis. Although extracellular vesicles (EVs)-based cell-to-cell communication mediates glioma progression, the key molecular mediators of this process are still not fully understood. Herein, we elucidated an EVs-mediated transfer of suprabasin (SBSN), leading to the aggressiveness and progression of glioma. High levels of SBSN were positively correlated with clinical grade, predicting poor clinical prognosis of patients. Upregulation of SBSN promoted, while silencing of SBSN suppressed tumorigenesis and aggressiveness of glioma cells in vivo. EVs-mediated transfer of SBSN resulted in an increase in SBSN levels, which promoted the aggressiveness of glioma cells by enhancing migration, invasion, and angiogenesis of recipient glioma cells. Mechanistically, SBSN activated NF-κB signaling by interacting with annexin A1, which further induced Lys63-linked and Met1-linear polyubiquitination of NF-κB essential modulator (NEMO). In conclusion, the communication of SBSN-containing EVs within glioma cells drives the formation and development of tumors by activating NF-κB pathway, which may provide potential therapeutic target for clinical intervention in glioma.
|WOS Accession No|
|ESI Research Field|
MOLECULAR BIOLOGY & GENETICS
Cited Times [WOS]:0
|Document Type||Journal Article|
|Department||Southern University of Science and Technology Hospital|
1.Affiliated Cancer Hospital & Institute of Guangzhou Medical University,Guangzhou,510095,China
2.Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation,School of Basic Medical Science,Guangzhou Medical University,Guangzhou,511436,China
3.Medical Research Center,Southern University of Science and Technology Hospital,Shenzhen,518055,China
4.Meishan Women and Children’s Hospital,Alliance Hospital of West China Second University Hospital,Sichuan University,Meishan,620000,China
5.Department of oncology,Huanggang Central Hospital of Yangtze University,Huanggang,438000,China
6.The Sixth Affiliated Hospital of Guangzhou Medical University,Qingyuan People’s Hospital,Guangzhou,511518,China
7.Department of Operating Room,Shenzhen Baoan Women’s and Childiren’s Hospital,Shenzhen,518000,China
8.Department of Urologic Oncosurgery,Affiliated Cancer Hospital & Institute of Guangzhou Medical University,Guangzhou,510095,China
9.Department of Pathogen Biology and Immunology,School of Basic Courses,Guangdong Pharmaceutical University,Guangzhou,510006,China
10.Department of Surgery,UT Southwestern Medical Center,Dallas,75390,United States
Chen，Han,Chen，Xuhong,Zhang，Zhuojun,et al. Extracellular vesicles-transferred SBSN drives glioma aggressiveness by activating NF-κB via ANXA1-dependent ubiquitination of NEMO[J]. ONCOGENE,2022,41(49):5253-5265.
Chen，Han.,Chen，Xuhong.,Zhang，Zhuojun.,Bao，Wenhao.,Gao，Zhiqing.,...&Jiang，Lili.(2022).Extracellular vesicles-transferred SBSN drives glioma aggressiveness by activating NF-κB via ANXA1-dependent ubiquitination of NEMO.ONCOGENE,41(49),5253-5265.
Chen，Han,et al."Extracellular vesicles-transferred SBSN drives glioma aggressiveness by activating NF-κB via ANXA1-dependent ubiquitination of NEMO".ONCOGENE 41.49(2022):5253-5265.
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