{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE302nnn/GSE302728/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"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=GSE302728"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"miR-30d suppresses innate immune signaling in cancer cells by attenuating the cGAS/STING/IFN-I cascade via a LATS2/YAP axis","description":"In cancer cells, miR-30d expression is cooperatively induced by HIF1α and missense mutp53 oncoproteins in response to hypoxia and ECM stiffness. In turn, miR-30d remodels the secretory pathway, particularly by promoting Golgi tubulo-vesiculation, leading to the release of a malignant secretome that drives ECM stiffening, CAF activation, and angiogenesis both at primary tumor sites and premetastatic niches.To investigate the impact of miR-30d inhibition on gene expression in early BC, we performed RNA-seq in MCF10 DCIS (MCF10DCIS.com cell line) cells treated with LNA-30d or control.","dates":{"publication":"2026/09/18"},"accession":"GSE302728","cross_references":{"GSM":["GSM9110398","GSM9110399","GSM9110397","GSM9110402","GSM9110400","GSM9110401"],"GPL":["24676"],"GSE":["302728"],"taxon":["Homo sapiens"]}}