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Psoriasis susceptibility-related RNA gene induced by stress (PRINS) is a long non-coding RNA (lncRNA) located on chromosome 4q22 (NCBI Gene ID: 541468). It was initially identified due to its significantly elevated expression in the non-lesional skin of patients with psoriasis, suggesting it plays a role in the genetic predisposition to the disease (Sonkoly et al., 2005, J Biol Chem). PRINS is induced by various cellular stressors, such as ultraviolet radiation and viral infections, and acts as a critical regulator of the keratinocyte stress response and apoptosis (Szegedi et al., 2010, J Invest Dermatol). It exerts its biological effects by modulating the expression of the anti-apoptotic gene G1P3 (also known as IFI6) and by physically interacting with proteins like nucleophosmin (NPM1) to maintain cellular homeostasis (Bari et al., 2011, FEBS Lett). In psoriasis, the dysregulation of PRINS contributes to the characteristic hyperproliferation of keratinocytes and the maintenance of a pro-inflammatory environment. Beyond inflammatory skin disorders, PRINS has been implicated in the progression of several malignancies, including breast and hepatocellular carcinoma, where it can influence tumor cell survival and metastasis (Zheng et al., 2019, Aging). Although no drugs targeting PRINS are currently FDA-approved, it is an active area of research for the development of RNA-based therapies, such as antisense oligonucleotides, aimed at treating chronic inflammatory conditions and cancer.
PRINS functions as a regulatory molecule that modulates the cellular stress response by controlling the expression of the anti-apoptotic gene G1P3 (IFI6) and interacting with the protein nucleophosmin (NPM1) to influence cell survival and inflammatory signaling.
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