{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE243nnn/GSE243084/"]},"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=GSE243084"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"High-Throughput Screening of Cancer Cluster Metastasis Inhibitors [Human]","description":"Extravasation is a pivotal step in cancer metastasis, however, no molecular control of cancer extravasation has yet been achieved because the mechanism behind this process remain poorly understood. Here, we identify Bay 61-3606 as cancer extravasation inhibitor using high throughput drug screening. Bay 61-3606 significantly decreases cancer cluster extravasation, which is associated with higher metastasis potential, in a zebrafish model. This inhibitory effect extends to decreased distant metastasis in a murine lung carcinoma model and a triple-negative breast cancer model. In addition, our RNA-sequencing results reveal the essential role of COL8A1, a cell-adhesion related molecule expressed by the extravasation participating endothelial cells, in cancer cluster extravasation. Bay 61-3606 treatment effectively decreases COL8A1 through JNK signaling pathway, resulting in impaired cancer cluster extravasation. As the infiltration of immune cells is independent on COL8A1, our findings suggest Bay 61-3606 is a potent drug for anti-metastasis therapy.","dates":{"publication":"2026/08/26"},"accession":"GSE243084","cross_references":{"GSM":["GSM7779101","GSM7779100","GSM7779099","GSM7779102"],"GPL":["24676"],"GSE":["243084"],"taxon":["Homo sapiens"],"PMID":["[42616881]"]}}