{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPCLAF, also known as p15(PAF), KIAA0101, or NS5ATP9, is an intrinsically disordered protein that binds the proliferating cell nuclear antigen (PCNA) and plays a central role in DNA replication and repair. Its conserved PCNA‐interacting (PIP) motif allows PCLAF to engage with the PCNA sliding clamp, thereby regulating processes such as replicative synthesis, translesion DNA repair and the bypass of replication‐fork–blocking lesions. Dynamic modifications—for example, the double mono‐ubiquitylation of PCLAF in response to DNA damage – trigger its timely removal from PCNA to ensure proper lesion bypass and maintain genomic integrity. Structural studies have further revealed that PCLAF not only binds the front face of PCNA but also traverses its inner channel, acting like a flexible “belt” that modulates clamp processivity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its functions in DNA metabolism, PCLAF is tightly regulated during the cell cycle and plays a significant role in oncogenic signaling. Its expression is controlled, in part, by APC/C‐mediated degradation and the Rb/E2F transcriptional axis—with levels peaking during S and G2 phases—to facilitate both proper cell cycle progression and DNA synthesis. PCLAF influences several key signaling pathways including Wnt/β‐catenin, MAPK and PI3K/AKT/mTOR, and it has been implicated in maintaining cancer cell stemness, centrosome homeostasis and resistance to apoptosis and chemotherapeutic agents. Aberrant elevation of PCLAF promotes tumor progression in a wide variety of cancers—such as colon, breast, adrenocortical, esophageal, pancreatic, and gliomas—by mechanisms that include the transcriptional activation of genes like c‐Myc and modulation of downstream effectors."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, the regulation of PCLAF by microRNAs, alternative splicing and associated noncoding RNA networks underscores its clinical relevance as both a prognostic biomarker and a therapeutic target. Elevated expression of PCLAF in tumor tissues and even in peripheral blood cells has been correlated with advanced disease stage, metastasis and poor overall survival in hepatocellular, gastric and non–small cell lung cancers. Regulatory axes involving miR-30a-5p, miR-1216a-15p and circRNA networks—as well as interactions with mitotic factors such as UbcH10—offer potential avenues for targeted intervention. In rectal and ovarian cancers, modulation of PCLAF not only influences radiotherapy sensitivity and chemoresistance but also impacts cell cycle progression and cancer stem cell self-renewal, providing preclinical evidence that the PCLAF signaling axis may represent a promising target in cancer therapy."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Lou K Povlsen, Petra Beli, Sebastian A Wagner, et al. 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