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Hypermethylation and low expression of FOXM1 predisposes women to unexplained recurrent miscarriage by impairing trophoblast stem cell proliferation. | LitMetric

AI Article Synopsis

  • Recurrent miscarriage (RM) is a challenging pregnancy issue, and researchers suggest that dysfunctional human trophoblast stem cells (hTSCs) might be involved, although the exact causes are still unclear.
  • This study identifies Forkhead box M1 (FOXM1) as a potential key factor linked to RM, highlighting its role as a transcription factor necessary for hTSC function, though its specific effects in this context are not fully understood.
  • The research shows that FOXM1 is more highly expressed in certain types of trophoblasts associated with growth and that its lower levels are correlated with RM, indicating that FOXM1 may influence important processes like cell proliferation and the cell cycle via transcriptional regulation.

Article Abstract

Recurrent miscarriage (RM) is a distressing pregnancy complication with an unknown etiology. Increasing evidence indicates the relevance of dysregulation of human trophoblast stem cells (hTSCs), which may play a role in the development of RM. However, the potential molecular regulatory mechanism underlying the initiation and maintenance of hTSCs is yet to be fully elucidated. In this study, we performed data analysis and identified Forkhead box M1 (FOXM1) as a potential factor associated with RM. FOXM1 is a typical transcription factor known for its involvement in various pathophysiological processes, while the precise function of FOXM1 functions in hTSCs and RM remains incompletely understood. Utilizing RNA-seq, CUT&Tag, ChIP-qPCR, and sodium bisulfite conversion methods for methylation analysis, we elucidate the underlying regulatory mechanisms of FOXM1 in hTSCs and its implications in RM. Our findings demonstrate the relative high expression of FOXM1 in proliferating cytotrophoblasts (CTBs) compared to differentiated extravillous cytotrophoblasts (EVTs) and syncytiotrophoblasts (STBs). Besides, we provide evidence supporting a significant correlation between FOXM1 downregulation and the incidence of RM. Furthermore, we demonstrate the significant role of FOXM1 in regulating hTSCs proliferation and cell cycle through the transcriptional regulation of CDKN3, CCNB2, CCNA2, MAD2L1 and CDC25C. Notably, we observed a correlation between the downregulation of FOXM1 in RM and hypermethylation in its promoter region. Collectively, these results provide insights into the impact of FOXM1 on trophoblast regulation and offer a novel perspective on RM.

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Source
http://dx.doi.org/10.1016/j.cellsig.2024.111259DOI Listing

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