{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe SKIL gene encodes the SNON protein, a multifunctional transcriptional regulator that is best known as a modulator of transforming growth factor‐β (TGF‑β)/Smad signaling. SNON exerts this function by binding to Smad proteins and either repressing or, in some cellular contexts, positively mediating TGF‑β transcriptional responses. In many studies, SNON has been shown to be subject to rapid degradation by Arkadia‐dependent ubiquitination in response to TGF‑β, while under other conditions its stability and function are modulated by post‑translational modifications such as sumoylation by enzymes like PIAS1 and TIF1γ. In addition, the subcellular localization of SNON – with nuclear SNON blocking Smad activity and cytoplasmic SNON sequestering Smads – contributes to its context‑dependent regulatory roles, influencing cell cycle arrest, differentiation, and extracellular matrix gene expression as part of the TGF‑β response."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its canonical role in TGF‑β signaling, SNON plays key roles in cell fate determination during development and in the epithelial–mesenchymal transition (EMT) process. In embryonic stem cells, for example, SNON associates predominantly with Smad2 at promoters of genes that regulate primitive streak formation and endoderm specification, influencing pluripotency and lineage commitment. In chondrocytes, SNON mediates a negative feedback loop that limits BMP signaling and subsequent hypertrophic maturation, while in various epithelial contexts SNON—through modulation of factors such as SLUG and by undergoing regulatory sumoylation—affects cell invasion, differentiation and even senescence. Furthermore, genomic studies have revealed that alterations in SKIL (including gene amplifications and chromosomal rearrangements) can add oncogenic potential by promoting cell invasion, and disrupting normal TGF‑β–mediated growth control."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn cancer, deregulation of SKIL/SNON contributes to a spectrum of oncogenic processes. In prostate cancer, rearrangements juxtaposing SKIL with androgen‐regulated promoters lead to its overexpression and increased invasiveness, while in non–small cell lung cancer SKIL has been implicated in promoting tumorigenesis and immune escape by modulating downstream effectors such as TAZ and autophagy. Moreover, SKIL is involved in post‑transcriptional regulatory networks—as highlighted in colorectal and other cancers—where its dysregulation can impact EMT, metastasis and even responses to therapy. Recent genome‐wide association studies have additionally linked variants in SKIL to drug‐induced cardiac effects, emphasizing the broad clinical impact of altered SKIL function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "29", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jun He, Sarah B Tegen, Ariel R Krawitz, et al. 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