GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE305nnn/GSE305941/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE305941GEOGSEfalseEffect of upregulation of MiR-29c-3p on gene expression during proliferation and metastasis of gastric cancer cellsMiR-29c-3p functions as a critical tumor suppressor in gastric cancer (GC) pathogenesis. Restoration of MiR-29c-3p expression significantly suppresses cellular proliferation, migration, and invasion, while inducing apoptosis and G1 phase arrest in GC cells. Transcriptomic profiling reveals that MiR-29c-3p modulates genes involved in signal transduction, angiogenesis, and extracellular matrix reorganization, primarily through inhibition of the PI3K/AKT signaling cascade. Mechanistically, MiR-29c-3p directly targets the SLC6A14 oncogene, as validated by RNA pull-down and dual-luciferase assays. This targeting is essential for MiR-29c-3p’s tumor-suppressive function: suppression of SLC6A14 blocks epithelial-mesenchymal transition (EMT) and inactivates PI3K/pAKT signaling in GC cells. Both in vitro and in vivo models confirm that MiR-29c-3p upregulation inhibits tumor progression via the SLC6A14-PI3K/AKT axis. Our findings establish a molecular framework wherein MiR-29c-3p antagonizes GC progression by directly repressing SLC6A14 and its downstream PI3K/AKT pathway, positioning MiR-29c-3p as a potential therapeutic target in GC management.2026/08/25GSE305941GSM9188331GSM9188332GSM9188333GSM9188334GSM9188335GSM9188336GSM9188337GSM9188338GSM9188339GSM9188329GSM9188340GSM918833029480305941Homo sapiens