{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nLong non‐coding RNA PANDAR (promoter of CDKN1A antisense DNA damage activated RNA) was initially identified as a DNA damage–inducible transcript that modulates cell fate by interacting with key transcription factors. In particular, PANDAR has been shown to bind nuclear factor-Y subunit A (NF‐YA) and influence p53 function, thereby regulating the transcription of genes critical for cell cycle control and apoptosis. Moreover, recent studies indicate that PANDAR can interact with RNA binding proteins such as PTBP1 to affect alternative splicing of apoptosis‐related transcripts."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the oncologic setting, aberrant PANDAR expression has been repeatedly linked to tumor progression and poor clinical outcomes across multiple cancer types. For example, in gastric cancer PANDAR is upregulated and promotes tumor advancement by competitively binding to p53, thereby down‐regulating the CDKN1A gene and facilitating cell cycle progression. In ovarian cancer, elevated PANDAR contributes to cisplatin resistance through a feedback loop involving the splicing factor SFRS2 and reduced p53 phosphorylation. Similarly, increased expression of PANDAR has been reported in hepatocellular carcinoma (where contrasting roles have been observed), glioma, pancreatic ductal adenocarcinoma, breast cancer, as well as in colorectal, bladder, and cervical cancers, with higher levels correlating with aggressive tumor behavior and unfavorable patient prognosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "3", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cancer, PANDAR also emerges as a regulator of cellular senescence and metabolic homeostasis. In adipocyte precursor cells, progressive upregulation of PANDAR—facilitated by promoter hypomethylation—is associated with early senescence and may contribute to the deterioration of glucose tolerance observed in obesity progressing toward type 2 diabetes. In combination with meta‐analyses that affirm its prognostic significance in diverse malignancies, these findings underscore the multifaceted impact of PANDAR in modulating cell survival, proliferation, and fate decisions in both oncologic and metabolic disorders."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yojiro Kotake, Kyoko Kitagawa, Tatsuya Ohhata, et al. 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