{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE342nnn/GSE342138/"]},"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=GSE342138"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Synthesis and Mechanistic Dissection of Biselyngbyaside Induced Cytotoxicity through Multi-omics Profiling","description":"Deciphering the mechanism of action of natural products remains great challenges. Biselyngbyasides (BILs), a class of marine 18-membered macrolides, display strong cytotoxicity in various cancer cells, whereas, their molecular mechanisms remain poorly understood. Here, we establish a multi-omics strategy integrating chemotranscriptomics, phosphoproteomics and peptide-centric local stability assays (PELSA) to systematically characterize cellular responses triggered by biselyngbyolide A (BILA). Multi-omics data analysis demonstrates that BILA triggered a signaling cascade including ER stress, UPR activation, lipid metabolism remodeling, cell-cycle arrest, and apoptosis by inhibition of SERCA. Using synthetic BILA and its aza-analogue, we performed structure-function analysis and further pinpoint the core pharmacophore responsible for cytotoxicity. This study clarifies the full signaling network regulated by BILA and provides a versatile analytical tools for mechanistic investigation of complex natural products in early drug discovery.","dates":{"publication":"2026/08/31"},"accession":"GSE342138","cross_references":{"GSM":["GSM9923736","GSM9923737","GSM9923738","GSM9923739","GSM9923740","GSM9923741","GSM9923742","GSM9923743","GSM9923744"],"GPL":["24676"],"GSE":["342138"],"taxon":["Homo sapiens"]}}