Overexpression of SHCBP1 promotes migration and invasion in gliomas by activating the NF‐κB signaling pathway
Citations Over TimeTop 17% of 2018 papers
Abstract
Gliomas are common, aggressive central nervous system tumors with poor overall survival rates. Despite improvements in neurosurgery, chemotherapy, and radiotherapy, the outcomes of patients with malignant gliomas remain poor. Therefore, increased knowledge of the molecular mechanisms that regulate glioma progression is crucial to identify novel therapeutic targets. Here, we reported that SHCBP1, a member of Src homolog and collagen homolog (Shc) family, was significantly overexpressed in glioma tissues and glioma cell lines compared to the corresponding normal tissues and cells. Ectopic overexpression of SHCBP1 promoted glioma cell migration and invasion, whereas knockdown of endogenous SHCBP1 had the opposite effects. Importantly, we demonstrated that SHCBP1 promoted aggressiveness in gliomas by activating the NF-κB signaling pathway. Collectively, our study indicates that SHCBP1 plays a pivotal role to promote progression in gliomas and targeting the oncogenic effects of SHCBP1 may provide a clinical strategy to treat gliomas.
Related Papers
- → Knockdown of LIMD2 inhibits the progression of ovarian carcinoma through ERK1/2 pathway(2023)2 cited
- → RNaseH-mediated simultaneous piggyback knockdown of multiple genes in adult zebrafish(2020)16 cited
- → Knockdown of ecdysteroid synthesis genes results in impaired molting and high mortality in Bactericera cockerelli (Hemiptera: Triozidae)(2022)9 cited
- → Supplementary Revised Figure S3 from MUC16 Regulates TSPYL5 for Lung Cancer Cell Growth and Chemoresistance by Suppressing p53(2023)
- → Supplementary Revised Figure S3 from MUC16 Regulates TSPYL5 for Lung Cancer Cell Growth and Chemoresistance by Suppressing p53(2023)