gp96 knockdown inhibits the malignant behaviors of glioblastoma cells by suppressing the NF-κB pathway

Clicks: 11
ID: 333220
2026
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #46 of 54 articles by views in Journal of Neuropathology & Experimental Neurology

Most read Least read

Bar heights use a square-root scale.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Abstract Glioblastoma (GBM) is the most aggressive primary brain tumor and has a dismal prognosis. The chaperone protein gp96 is implicated in various cancers but its role and functions in GBM remain poorly defined. This study aimed to investigate the expression, function, and underlying mechanism of gp96 in GBM pathogenesis. gp96 expression was analyzed via the GEPIA2 database. The cell counting kit-8, EdU staining, colony formation and transwell assays were performed to evaluate viability, proliferation, invasion and migration of GBM cell lines. The underlying mechanism was investigated by Kyoto Encyclopedia of Genes and Genomes analysis and Western blot. The results showed that gp96 mRNA and protein levels were upregulated in GBM cells and that gp96 knockdown significantly inhibited viability, proliferation, migration and invasion by the cells. gp96 was found to be enriched in the NF-κB pathway and gp96 knockdown inhibited NF-κB pathway activation in the GBM cells. The NF-κB activator phorbol 12-myristate 13-acetate restored the viability, proliferation, migration, and invasion inhibited by gp96 knockdown. Thus, our findings revealed that gp96 knockdown inhibited the malignant behaviors of GBM by suppressing the NF-κB pathway. This study identifies the gp96/NF-κB axis as a novel potential therapeutic target for GBM intervention.
Reference Key
openalex_W7223088863 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Chengshi Lin, Pingqing Lin, Nengping Huang, Jun Min, Liang Chen, Yongqing Ye
Are you one of these authors? Claim your profile
Journal Journal of Neuropathology & Experimental Neurology
Year 2026
DOI
10.1093/jnen/nlag111
URL
https://doi.org/10.1093/jnen/nlag111
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.