Transcriptomic analysis of hormone-sensitive patient-derived endometrial cancer spheroid culture defines Efp as a proliferation modulator

Estrogen-responsive endometrial cancer (EC) is prevalent in uterine cancer. Its precise molecular mechanisms remain to be elucidated partly because of limited availability estrogen-sensitive EC models recapitulating clinical pathophysiology. We previously established patient-derived cell (EC-PDC) spheroid culture with high expression estrogen receptor α (ERα). Using this EC-PDC, we study the transcriptional regulation and function estrogen-responsive finger protein (Efp), a prototypic tripartite motif (TRIM) that modulates degradation RNA processing. Intense estrogen-dependent EFP mRNA induction ERα occupancy responsive element (ERE) were observed EC-PDC. Luciferase reporter gene assay showed ERE facilitates activity estrogen-dependently. siRNA-mediated Efp silencing EC-PDC resulted suppressed proliferation altered profile, featuring downregulation genes related cycle (e.g., CDK6) inflammation/immune responses IL10RA, IL26, IL6ST) while unaffected stemness-related markers. Taken together, powerful tool enables dissect Efp-mediated signaling pathways as an model. This provides insight into alternative therapeutic strategies targeting ERα-Efp axis.