{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nProgrammed cell death 5 (PDCD5) is emerging as a pivotal modulator of cellular stress responses through its ability to regulate apoptosis via the p53 network. Mechanistic studies have shown that PDCD5 physically interacts with key regulators—binding to the histone acetyltransferase Tip60 and directly associating with the N‐terminal domain of p53—to stabilize p53 by antagonizing Mdm2‐mediated ubiquitination, thereby promoting the transcription of pro‐apoptotic genes. In addition, PDCD5 is dynamically regulated by post‐translational modifications and interacting partners such as the deubiquitinase OTUD5, the co‐chaperone DNAJB1, and the phosphatase PPEF‐1, which modulate its stability and nuclear translocation in response to genotoxic stress. These findings, supported by computational modeling of its impact on p53 dynamics, underscore the dual role of PDCD5 in maintaining basal p53 levels during normal growth and in amplifying the apoptotic response after DNA damage."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAberrant PDCD5 expression has been observed in a wide array of human malignancies, where its downregulation is frequently associated with increased tumor aggressiveness, chemoresistance, and poor clinical outcomes. In gastric, leukemia, glioma, ovarian, prostate, and gastrointestinal stromal tumors, lower PDCD5 levels correlate with enhanced proliferative capacity and diminished apoptosis. Moreover, studies in hepatocellular carcinoma, serous cystadenocarcinoma, and chondrosarcoma indicate that restoration of PDCD5 expression can improve drug sensitivity and is linked to longer patient survival. Together, these findings support a tumor‐suppressive role for PDCD5 and highlight its potential as both a prognostic biomarker and a sensitizer to conventional chemotherapeutic agents."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in cancer biology, PDCD5 is implicated in diverse physiological and pathological processes including immune regulation, inflammatory arthritis, and tissue remodeling. Alterations in its expression and epigenetic modifications have been reported in autoimmune conditions such as rheumatoid arthritis, osteoarthritis, and psoriasis, while its promoter activity and structural features—such as a stable N‐terminal α‐helix—appear essential for its apoptotic function. Furthermore, PDCD5 has been associated with the modulation of protein folding (for example, by interfering with β‐tubulin maturation), and recent work has also linked its deregulation to cardiac remodeling and lung fibrosis. Collectively, this body of work posits PDCD5 as a multifaceted protein whose regulatory mechanisms not only determine cell fate decisions under stress but may also serve as promising therapeutic targets in both oncology and chronic inflammatory diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "29", "end_ref": "43"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Lanjun Xu, Yingyu Chen, Quansheng Song, et al. 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