{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE330nnn/GSE330529/"]},"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=GSE330529"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Transcriptomic Profiling Identifies GPNMB as a Key Driver of Gastric Cancer Aggressiveness","description":"We aimed to define the role of GPNMB in gastric cancer (GC) progression and its underlying mechanisms. Stable GPNMB-knockdown/overexpression GC cell models were established, and transcriptomic profiling identified the cAMP signaling pathway as a key downstream effector. GPNMB silencing significantly inhibited GC cell proliferation, invasion, induced G1 arrest and apoptosis, while overexpression activated the cAMP/PKA/CREB axis to upregulate c-Myc, Cyclin D1 and EMT markers, which was reversed by the PKA inhibitor H-89. GPNMB also promoted an immunosuppressive microenvironment via IL-6 and TGF-β upregulation and accelerated xenograft tumor growth. Our findings identify GPNMB as a critical driver of GC malignancy through the cAMP/PKA/CREB axis, representing a promising therapeutic target.","dates":{"publication":"2026/05/17"},"accession":"GSE330529","cross_references":{"GSM":["GSM9728226","GSM9728225","GSM9728228","GSM9728227","GSM9728224","GSM9728223"],"GPL":["24676"],"GSE":["330529"],"taxon":["Homo sapiens"]}}