IndraLab
Statements
"Mechanistically, we found that <span class="match term0">USP5</span> deubiquitinated <span class="match term1">BETA-CATENIN</span>, prevented ubiquitination mediated <span class="match term1">BETA-CATENIN</span> degradation and promoted <span class="match term1">BETA-CATENIN</span> nuclear accumulation, leading to the activation of Wnt/<span class="match term1">BETA-CATENIN</span> signal pathway in NSCLC cells"
reach
"Collectively, these data suggest that USP5 deubiquitinates β-catenin, promotes β-catenin stability, and subsequently promotes Wnt signaling pathway activity in lung cancer cells.To confirm the role of β-catenin in USP5-mediated stemness, we silenced the β-catenin expression in USP5-overexpressing A549 cells and determined the sphere-forming ability (Additional file 1: Figure S5D)."
reach
"Here, our findings provide new insights indicating that USP5 interacts with β-catenin, causes β-catenin deubiquitination, prolongs the β-catenin protein half-life, and thus increases the expression of Wnt/β-catenin downstream target genes in lung cancer.Our study showed WP1130 inhibited cell motility and cancer stemness in lung cancer."
reach
"Finally, we found that in breast cancer cells DEPDC1B mediates the deubiquitination of β-catenin by USP5, stabilizes the β-catenin protein level, promotes nuclear translocation, activates the wnt/β-catenin signaling pathway, and ultimately promotes the transfer of breast cancer cells (Fig. 8)."