{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPLAGL2 is a zinc finger transcription factor that has emerged as a critical regulator of cellular plasticity and oncogenesis. In malignant gliomas, for example, its amplification and overexpression inhibit neural stem cell differentiation while promoting self‐renewal, and in acute myeloid leukemia it cooperates with fusion oncoproteins to drive the expansion of progenitor cells. Moreover, in the intestinal epithelium PLAGL2 is targeted by Let‐7 microRNAs and, when derepressed, activates Wnt signaling and key stem cell transcription factors to reinforce an undifferentiated state—a mechanism also recapitulated in lung cancer stemness via E2F1‐mediated transcriptional activation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn a wide range of cancers—including colorectal, gastric, bladder, prostate, pediatric central nervous system tumors, and diffuse large B‐cell lymphoma—PLAGL2 overexpression has been closely linked to enhanced proliferation, migration, invasion, and epithelial–mesenchymal transition. By binding to promoters of targets such as Wnt6 in colorectal cancer and through its partnership with co‐oncogenic proteins, PLAGL2 not only influences cell‐cycle progression but also contributes to chemoresistance and aggressive metastatic behavior. Additionally, its aberrant activity is associated with distinct tumor subtypes, such as colorectal mucinous adenocarcinoma, underscoring its potential as both a biomarker and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the mechanistic level, PLAGL2 functions predominantly as a transcriptional activator by binding directly to promoter regions of key target genes. It regulates the expression of genes such as surfactant protein‐C in the lung (via direct promoter occupancy), and modulates the transcription of NCF2 in response to inflammatory stimuli. Its transcriptional activity is finely tuned by post‐translational modifications—acetylation by Tip60 can abrogate its SUMOylation—while interactions with proteins like Pirh2 and components of the Mediator complex (e.g., PC2) further influence its function. In addition, PLAGL2 regulates cytoskeletal dynamics by modulating small GTPases such as RhoA and Rac1 and, in certain contexts, can even trigger cell cycle arrest and apoptosis via p73, highlighting its multifaceted role in cellular regulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cancer, PLAGL2 is also implicated in non‐malignant biological processes. In the lung, for instance, it modulates surfactant protein‐C expression under conditions of oxidative stress and hypoxia, contributing to epithelial injury and pathological remodeling observed in emphysema. Furthermore, aberrant PLAGL2 activity has been linked to developmental disorders such as Hirschsprung disease, while microRNAs (for example, miR‑22‑3p) have been shown to target PLAGL2 to curb its pro‐migratory effects in breast cancer. These observations underscore the context‐dependent versatility of PLAGL2 in both development and disease."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Sean F Landrette, Ya-Huei Kuo, Karen Hensen, et al. 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