GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE329nnn/GSE329207/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE329207GEOGSEfalseTargeting phosphatidylserine for tumor cell suppression [RNA-seq]Alterations in lipid metabolism are frequently observed in cancers, playing a pivotal role in tumor cell survival and proliferation. Phosphatidylserine (PS), the most negatively charged glycerophospholipid in eukaryotic membranes, is synthesized in mammals by key enzymes, such as phosphatidylserine synthase 1 (PTDSS1). Here, we identify a PS-dependent metabolic vulnerability in esophageal squamous cell carcinoma (ESCC) and glioblastoma (GBM). Pharmacological inhibition of PTDSS1 potently suppresses tumor growth with nanomolar efficacy. Mechanistically, PS depletion causes a metabolic depletion of PS and phosphatidylethanolamine (PE), triggering endoplasmic reticulum (ER) stress and activating autophagy. These findings reveal an unrecognized PS-dependent metabolic dependency for tumor cell viability, indicating that targeting PS synthesis may offer a promising therapeutic approach for tumor cell suppression.2026/08/05GSE329207GSM9699261GSM9699260GSM9699270GSM9699259GSM9699269GSM9699268GSM9699267GSM9699266GSM9699265GSM9699264GSM9699263GSM969926224676329207Homo sapiens[42511570]