{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n The cancer‐testis paradigm, in which certain long non‐coding RNAs (lncRNAs) are expressed in both gametogenic and tumorigenic tissues, provides a context for evaluating the roles of specific lncRNAs such as DACT3‐AS1."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " Although abstract"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "does not mention DACT3‐AS1 explicitly, the work underscores the central functions that many lncRNAs have in regulating processes including telomere biology, chromatin dynamics, and signal transduction via pathways such as Wnt/β‐catenin and PI3K/AKT/mTOR—all processes in which DACT3‐AS1, as an antisense transcript to DACT3, is likely to be implicated. In many cancers, DACT3 (a known negative regulator of the Wnt pathway) and its associated antisense transcript DACT3‐AS1 are thought to act together to modulate gene expression epigenetically and thereby influence cell proliferation, migration, and immortalization. This dual role in both gametogenesis and tumorigenesis suggests that DACT3‐AS1 may contribute to the molecular programs of meiotic induction and immune evasion seen in tumors while also playing a role in the regulation of chromatin organization in testis-specific developmental contexts. In summary, DACT3‐AS1 is emerging as a potentially critical regulator within the shared networks that underpin both germ cell development and cancer progression, representing a promising candidate for biomarker development in early detection and therapeutic response monitoring.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ali Dianatpour, Soudeh Ghafouri-Fard "}, {"type": "b", "children": [{"type": "t", "text": "Long Non Coding RNA Expression Intersecting Cancer and Spermatogenesis: A Systematic Review"}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Asian Pac J Cancer Prev (2017)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.22034/APJCP.2017.18.10.2601"}], "href": "https://doi.org/10.22034/APJCP.2017.18.10.2601"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "29072050"}], "href": "https://pubmed.ncbi.nlm.nih.gov/29072050"}]}]}]}