Method Profile
Compare short drug-induced gene-expression responses across monolayers, cell-line assembloids and primary endometrial assembloids.
Proof-of-concept follow-up of transcriptomics-based endometriosis drug-repurposing candidates.
12Z epithelial/iEc stromal cell-line assembloids and primary eutopic endometrial epithelial/stromal assembloids from two patients.
Agarose-micromold 3D assembly followed by 24-hour exposure and bulk RNA sequencing. The drug-test method specifies 1:50 epithelial:stromal input for cell-line assembloids; cell-line histology uses 1:20. Primary-tissue seeding ratios were 3:1, 1:5, 1:10 and 1:20.
Cell systems
Epithelial and stromal monolayers; cell-line assembloids; primary endometrial assembloids from endometriosis patients.
Compounds and analysis
Ibuprofen 19.4 μM, fenoprofen 7.2 μM, simvastatin 9.6 μM, primaquine 8.8 μM; RNA-seq differential expression and pathway comparison with prior disease signatures.
Drug-induced gene expression and pathways are compared within each sample source, with separately reported sequencing-sample numbers.
Compare four drug responses across monolayer and assembloid sources.
Three samples per cell-line/drug condition; one per cell-line assembloid condition; two per primary assembloid condition from two patients.
DMSO within each sample source; prior endometriosis microarray signatures for pathway direction.
Simvastatin produced the broadest expression changes; primaquine and fenoprofen showed source-specific pathway effects; ibuprofen reversed no assessed disease pathway.
A preprint compares four drugs in epithelial and stromal monolayers, cell-line assembloids and primary endometrial assembloids. Simvastatin caused the broadest expression changes, but responses depended strongly on sample type and sequencing replication was limited.
