AI Article Synopsis
- Epithelial-to-mesenchymal transition (EMT) facilitates cancer cell invasion and migration, with a key focus on the role of FBXO11 in regulating ZEB1, a critical factor in EMT.* -
- FBXO11 promotes the degradation of ZEB1 through ubiquitination, and its depletion leads to ZEB1 accumulation, resulting in increased EMT and aggressiveness in non-small cell lung cancer (NSLC) cells.* -
- High levels of FBXO11 correlate with better prognosis in NSLC, suggesting its potential as a therapeutic target by modulating EMT and ZEB1 stability.*
Article Abstract
Epithelial-to-mesenchymal transition (EMT) affects the invasion and migration of cancer cells. Here, we show that FBXO11 recognizes and promotes ubiquitin-mediated degradation of ZEB1. There is a strong association between FBXO11 and ZEB1 in non-small cell lung cancer (NSLC) in a clinical database. FBXO11 interacts with ZEB1, a core inducer of EMT. FBXO11 leads to increased ubiquitination and proteasomal degradation of ZEB1. Depletion of endogenous FBXO11 causes ZEB1 protein accumulation and EMT in A549 and H1299 cells, while overexpression of FBXO11 reduces ZEB1 protein abundance and cellular invasiveness. Importantly, the depletion of ZEB1 suppresses the increased migration and invasion of A549 and H1299 cells promoted by the depletion of FBXO11. The same results are shown in xenograft tumors. High FBXO11 expression is associated with a favorable prognosis in NSLC. Collectively, our study demonstrates that FBXO11 modulates EMT by mediating the stability of ZEB1 in lung cancer cells.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11476264 | PMC |
| http://dx.doi.org/10.3390/cancers16193269 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!