<HashMap><database>GEO</database><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE319116</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>USP22 Facilitates Gastric Cancer Progression via Hippo/YAP axis</name><description>Gastric cancer (GC) is one of the most common malignancies in the digestive system. Previous studies demonstrated that the dysregulation of the Hippo pathway and hyperactivation of the YAP/TEAD transcriptional axis played important roles in GC progression, although the underlying mechanisms remain incompletely understood. Our study demonstrated that the deubiquitinase USP22 plays a pivotal role in regulating the Hippo pathway in GC, where its inhibition markedly suppresses YAP/TEAD activity and tumor progression. Mechanistically, USP22 interacts with YAP and inhibits its K48-linked polyubiquitination, thereby enhancing YAP protein stability and Hippo/YAP axis activity in GC. Intriguingly, YAP can transcriptionally upregulate USP22 by binding to its promoter region, establishing a positive feedback loop that promotes gastric cancer progression. Collectively, our findings reveal a reciprocal activation mechanism between USP22 and the Hippo pathway in gastric tumorigenesis, identifying USP22 as a promising novel therapeutic target.</description><dates><publication>2026/06/01</publication></dates><accession>GSE319116</accession><cross_references><GSM>GSM9511025</GSM><GSM>GSM9511026</GSM><GSM>GSM9511023</GSM><GSM>GSM9511024</GSM><GSM>GSM9511027</GSM><GSM>GSM9511028</GSM><GPL>24676</GPL><GSE>319116</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>