TGF‑β1 impairs CEP131‑dependent primary cilia assembly and decidualization in human endometrial stromal cells

Defective decidualization in endometriosis is linked to impaired endometrial receptivity, recurrent implantation failure, and adverse pregnancy outcomes, but how endometriosis-related inflammatory cytokines perturb endometrial stromal cells remains unclear. Here, we show that transforming growth factor‑β1 (TGF‑β1) disrupts CEP131‑dependent primary cilia assembly and thereby attenuates decidualization in human endometrial stromal cells. In vitro decidualization induced by medroxyprogesterone acetate (MPA) and cAMP promoted primary cilium formation, and selectively upregulated the centriolar satellite protein CEP131. Structurally, CEP131 accumulated at the basal body and along the ciliary axoneme. Depletion of CEP131 markedly reduced the proportion and length of primary cilia and diminished expression of decidual markers, indicating that CEP131 is required for efficient ciliogenesis and decidualization. Notably, CEP131 expression was downregulated in women with endometriosis. TGF‑β1, but not interleukin‑6, abrogated CEP131 expression, suppressed decidualization, and reduced cilia frequency and length. Disruption of centriolar satellite dynamics by PCM1 depletion, microtubule depolymerization, or dynactin disruption similarly prevented CEP131 aggregation, shortened cilia, and impaired decidualization, supporting a critical role for satellite‑mediated CEP131 assembly in primary ciliogenesis and decidualization. Mechanistically, cAMP–PKA signaling and a CDK2–PLK4 axis promoted CEP131 aggregation at primary cilia, whereas pharmacologic or genetic inhibition of CDK2 or PLK4 reduced CEP131 assembly, ciliary length, and decidual marker expression. Collectively, these findings identify CEP131‑dependent primary cilia as essential organizers of decidual signaling and reveal TGF‑β1 as a cytokine that compromises endometrial stromal cell decidualization by targeting this ciliogenic machinery.