Transcriptomic signature from G3BP2 knockdown versus control in endometrial stromal cells

to investigate the functional role of G3BP2, which is aberrantly overexpressed in endometriotic lesions, in regulating the molecular programs of endometrial stromal cells. By performing transcriptomic profiling following G3BP2 knockdown in endometrial stromal cells and comparing it with control cells, we seek to define G3BP2-dependent gene expression networks and biological pathways involved in lesion survival, metabolic adaptation, and disease progression. Elucidating the transcriptional consequences of G3BP2 depletion will provide mechanistic insights into how G3BP2 contributes to the pathogenesis of endometriosis and may identify potential therapeutic targets for limiting lesion growth and recurrence.