{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPDZ‐binding kinase (PBK/TOPK) is a serine/threonine kinase that is frequently overexpressed in many malignancies and plays multifaceted roles in tumor cell biology. It is activated during mitosis—often by upstream kinases such as CDK1/cyclin B1 and Src—and phosphorylates key substrates that govern cell‐cycle progression and cytokinesis. In several studies PBK was shown to promote transformation by suppressing the transcriptional activity of p53, phosphorylating proteins such as p97 and LGN to ensure proper abscission, and engaging in kinase cascades that enhance survival and proliferation. Moreover, its upregulation in hematologic neoplasms and solid tumors correlates with resistance to apoptosis, increased clonogenicity, and an ability to override DNA damage checkpoints, suggesting that PBK is an important driver of oncogenic cell cycle deregulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nPBK/TOPK also exerts a pivotal role in promoting tumor invasion, metastasis, and chemoresistance. It modulates multiple signaling axes—including those involving MAPKs, AKT, ERK, p38, and the β‐catenin–TCF/LEF pathway—to induce resistance to anoikis, enhance migratory and invasive capacities, and upregulate metastasis‐promoting effectors such as uPAR and matrix metalloproteinases. Elevated levels of PBK in cancers such as colorectal, gastric, lung, ovarian, and prostate carcinomas have been directly correlated with aggressive disease features, altered transcriptional programs, and poor prognostic outcomes. In addition, PBK facilitates epithelial–mesenchymal transition through augmenting transforming growth factor–β1/Smad signaling, further linking its activity to tumor progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its classical roles in cell division and metastatic behavior, PBK/TOPK is emerging as an attractive target for therapeutic intervention. Studies in neural progenitor cells reveal that it is a marker of transient amplifying populations and is essential for self‐renewal, while in inflammatory contexts PBK modulates NF‐κB and p38 signaling—thereby influencing both immune responses and tumor radiosensitivity. Moreover, small‐molecule inhibitors (and even natural compounds such as glycycoumarin) that target PBK have demonstrated efficacy in sensitizing tumor cells to chemotherapy and radiotherapy, as well as in suppressing tumor growth in vivo. These findings underscore the utility of PBK both as a prognostic biomarker and as a promising target for anticancer therapies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Asit Nandi, Michael Tidwell, Judith Karp, et al. 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