{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nFOXC1 is a pivotal forkhead transcription factor that orchestrates embryonic development with a critical role in the formation and differentiation of anterior segment tissues of the eye. Mutations, gene dosage alterations, and post‐translational modifications of FOXC1 result in a spectrum of ocular anomalies—including Axenfeld–Rieger syndrome and glaucoma—by disrupting mesenchyme–neuroepithelium interactions and impairing proper transcriptional regulation in the developing eye. In addition, aberrant FOXC1 function has been linked to other developmental defects such as cerebellar malformations and cerebrovascular instability, underscoring its essential role in maintaining ocular and vascular homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of cancer, FOXC1 is frequently overexpressed and has emerged as a robust biomarker and functional driver in numerous aggressive malignancies such as basal‐like/triple‐negative breast cancer, colorectal, endometrial, non‐small cell lung, pancreatic, and oral squamous cell carcinomas. It promotes oncogenic processes by enhancing cell proliferation, migration, invasion, and epithelial–mesenchymal transition through transcriptional activation of downstream effectors (for example, matrix metalloproteinase 7), modulation of non‐canonical Hedgehog and NF‑κB signaling, and facilitating cancer stem cell–like properties. Moreover, FOXC1 itself is subject to regulation by noncoding RNAs—including microRNAs (miR‑495, miR‑138, miR‑204) and long noncoding RNAs (e.g. FOXCUT) as well as circular RNAs—all of which fine‑tune its expression and thereby critically influence tumor aggressiveness and metastatic potential. 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