{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPIWIL1 (also known as HIWI) is a highly conserved member of the PIWI subfamily that plays an essential role in normal germline physiology. In human testes, PIWIL1 is selectively expressed in spermatogenic cells such as spermatocytes and round spermatids, where it helps maintain genomic stability through transposon silencing and supports germ cell proliferation. Moreover, germline mutations that prevent its proper ubiquitination and degradation disrupt the histone‐to‐protamine exchange during spermiogenesis, ultimately contributing to male infertility."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its physiological role, aberrant re‐expression and overexpression of PIWIL1 have been reported in a wide spectrum of human cancers—including those of the stomach, soft tissue, lung, brain, colorectum, liver, endometrium, breast, kidney, and cervix—where its high levels correlate with aggressive tumor behavior and poorer clinical outcomes. In these malignancies, PIWIL1 enhances oncogenic properties by promoting cell proliferation, migration, invasion, and self‑renewal. Its increased expression is associated with deregulated cell‐cycle progression, epigenetic alterations (for example, DNMT1‑mediated hypermethylation leading to silencing of tumor suppressors such as PTEN), and resistance to chemotherapy. Such oncogenic functions have positioned PIWIL1 as both a prognostic biomarker and a potential target for anticancer therapy."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "25"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nRecent studies have revealed that PIWIL1 can also exert oncogenic effects through alternative, piRNA‐independent mechanisms. In certain tumors, PIWIL1 functions as a co‑activator of the anaphase promoting complex/cyclosome to target substrates involved in cell adhesion and metastasis, and it may interface with mRNA decay pathways (such as via UPF1) to regulate transcript stability. Structural investigations have further uncovered non‑canonical interactions between PIWIL1 and Tudor domain–containing proteins, illustrating its versatile role in RNA‑mediated gene regulation. Functional experiments employing CRISPR‑Cas9–mediated knockout have demonstrated that loss of PIWIL1 significantly impairs tumor cell proliferation, migration, and in vivo tumor growth, while also modulating tumor metabolism and immune cell recruitment."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "32"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Dan Qiao, Anne-Marie Zeeman, Wei Deng, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "Genetic variants in Piwi-interacting RNA pathway genes confer susceptibility to spermatogenic failure in a Chinese population."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Hum Reprod (2010)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1093/humrep/deq274"}], "href": "https://doi.org/10.1093/humrep/deq274"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "20940137"}], "href": "https://pubmed.ncbi.nlm.nih.gov/20940137"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Lan-Tao Gou, Jun-Yan Kang, Peng Dai, et al. 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