{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE319nnn/GSE319116/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE319116"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"USP22 Facilitates Gastric Cancer Progression via Hippo/YAP axis","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.","dates":{"publication":"2026/06/01"},"accession":"GSE319116","cross_references":{"GSM":["GSM9511025","GSM9511026","GSM9511023","GSM9511024","GSM9511027","GSM9511028"],"GPL":["24676"],"GSE":["319116"],"taxon":["Homo sapiens"]}}