{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nZNF143 is a zinc‐finger transcription factor that functions as an essential architectural and regulatory protein by binding sequence‐specific DNA elements at gene promoters and distal regulatory regions. It participates in the establishment of chromatin loops and promoter–enhancer contacts, thereby ensuring proper stimulus‐ and lineage‐specific transcription. In several studies, ZNF143 was shown to occupy anchor sites of chromatin interactions, acting in concert with other factors such as HCFC1 and THAP11 to regulate expression from CpG‐rich promoters and to provide sequence specificity to the basal transcription machinery. Its ability to directly bind cisplatin–modified DNA further underscores its involvement in the cellular response to DNA damage and genome organization."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its architectural role, ZNF143 regulates critical cell‐cycle and DNA repair genes, thereby impacting cell proliferation and chemoresistance. For example, its regulatory activity underlies the transcription of genes such as CDC6, PLK1, MCM family proteins, as well as Rad51 and flap endonuclease‐1, which are linked to both cell-cycle progression and effective DNA repair. Moreover, altered ZNF143 expression has been associated with resistance to cisplatin in various cancer cells, and its overexpression correlates with poor prognosis in hepatocellular, gastric, and colon cancers. Consistent with this, its modulation can influence epithelial–mesenchymal transition and migratory behavior, emphasizing ZNF143’s role as a master regulator of oncogenic cell growth."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in chromatin architecture and cell‐cycle regulation, ZNF143 participates in a broader transcriptional regulatory network that influences diverse cellular processes. It is involved in regulating tissue‐specific metabolic genes, including those for mitochondrial transcription (via TFAM) and antioxidant enzymes, and it contributes to mitotic bookmarking by maintaining association with chromatin during cell division. Through interactions with other transcriptional regulators, ZNF143 also modulates inflammatory responses and cytokine secretion (for instance, IL‑8), and its activity is implicated in the regulation of genes involved in stress responses. These functions extend to the regulation of genes controlling cell motility and intercellular signaling and even to the modulation of stem‐cell phenotypes via cooperation with factors such as LIN28B, highlighting its pleiotropic role in both normal physiology and cancer progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFurthermore, emerging evidence highlights the involvement of ZNF143 in the modulation of tissue‐specific differentiation and tumor microenvironment dynamics. In bone biology, for instance, its interplay with factors like ATF4 and FIAT modulates osteoblast activity and bone mass accrual, while in diverse tumor settings—including glioma, lung adenocarcinoma, and cervical cancer—ZNF143 regulates oncogenic pathways via interactions with proteins such as KPNA2, E6–AP, and others to promote proliferation, migration, and therapy resistance. These findings position ZNF143 as a promising target for therapeutic intervention in cancer and other diseases characterized by aberrant transcriptional regulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Swneke D Bailey, Xiaoyang Zhang, Kinjal Desai, et al. 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