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BRCA1 pseudogene 1 (BRCA1P1) is a transcribed pseudogene derived from the BRCA1 tumor suppressor gene, containing only three of the 24 exons of BRCA1 and also featuring sequence insertions from the RPLP1 ribosomal protein pseudogene[1][4][7]. Due to a point mutation at the translation start site, BRCA1P1 does not encode a protein but instead produces a long non-coding RNA (lncRNA) that accumulates in the nucleus and is ubiquitously transcribed in human tissues, with increased expression in breast cancer[1][3][7]. The lncRNA transcribed from BRCA1P1 has been shown to bind the NF-κB subunit RelA, resulting in negative regulation of antiviral gene expression and suppression of cytokine production; conversely, knockout or depletion of BRCA1P1 activates an antiviral-like innate immune response and suppresses tumor growth in breast cancer models[3][4][7][8][9]. BRCA1P1 is implicated in the modulation of tumor immunity and may participate in neoplastic processes, with genomic amplification events in breast tumors suggesting a possible contribution to tumorigenesis[1][3]. No drugs or therapeutic interventions currently target BRCA1P1 directly, nor is it considered a receptor, enzyme, transporter, or canonical druggable target. Current evidence highlights BRCA1P1 mainly as a regulatory non-coding RNA of potential relevance for cancer biology and immunity, but not as a conventional therapeutic target[3][4][7].
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