FOXP1 (Forkhead Box P1)

These multi-layered analyses provide novel insights into epigenetic mechanisms underlying OL to OSCC progression and highlight candidate biomarkers with strong translational potential. By combining IML based methylation modeling with external and cross-omics validation, this study advances the development of reliable, interpretable biomarkers for precision oral cancer diagnostics and management.

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Radiation-induced DYNLL1-AS1 in ESCC EVs drives PD-L1⁺ TAMs immunosuppression via SEC22B/ FOXP1 signaling. Combining DYNLL1-AS1 inhibition with PD-L1 blockade may reverse RT-induced immunosuppression, offering a transformative strategy for ESCC radio-immunotherapy.

The IC50 value for AChE inhibition by the extract was 0.113 ± 0.010 µg/mL, which is approximately 1.8-fold higher than that of the standard inhibitor, donepezil (0.061 ± 0.009 µg/mL), indicating considerable AChE inhibition. crepidiodes extract's HPLC-identified components, chlorogenic acid and ellagic acid, demonstrated high binding profile and stability with GATA2 and FOXP1 targets, supporting the in vivo antifibrotic activity of this plant. Hence, C. crepidiodes may have intricate effects on the molecular pathways linked to uterine fibroids, such as re-establishing normal ovarian morphology, hormone balance, and insulin sensitivity.

The findings elucidated genetic associations between SCZ and BC and identified critical shared genetic contributors, thereby offering molecular evidence for the investigation of comorbidity mechanisms and potential intervention strategies.

FOXP1 promoted the Wnt/β-catenin pathway by regulating AEG-1. Overall, overexpressing FOXP1 drives stem cell properties and radioresistance of HCC cells by promoting AEG-1-mediated Wnt/β-catenin pathway, providing a promising therapeutic target for enhancing radiotherapy efficacy.

P=N/A, N=12, Not yet recruiting, Dr Ruth Braden - The University of Melbourne

This degradation relieves FOXP1 repression of Cyclin E2, promoting CRC cell proliferation. In summary, FBXO44 is an oncogene that promotes CRC tumorigenesis by degrading FOXP1 and upregulating Cyclin E2, offering a potential therapeutic target for CRC.

Mechanistically, rs10871066 triggers silencer-to-enhancer switching mediated by FOXP1 and TCF7L2, distally upregulating KLF5 to activate oncogenic pathways and PIBF1 to suppress natural killer cell cytotoxicity. Our study provides a comprehensive resource of dynamic epigenomic atlas, a functionally informed PRS for risk prediction and insights into epigenetic mechanisms underlying CRC development.

Mechanistically, ZC3H13 stabilizes FOXP1 expression via m6A methylation, driving metabolic reprogramming. These findings uncover a novel ZC3H13-FOXP1 axis and suggest potential therapeutic targets for AML treatment.

Functionally, the knockdown of FOXP1 demonstrated antileukemic effects, including reduced AML cell proliferation and cell cycle arrest in the G1-S phase. In conclusion, this study systematically investigated the role of FOXP1 across a spectrum of hematological malignancies and demonstrated that FOXP1 was a promising prognostic biomarker and a potential therapeutic target in AML and other hematological malignancies.

We have constructed an angiogenesis-related gene prognostic signature that enriches the prognostic assessment system for AML and provides novel therapeutic directions for this disease.