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Programmed cell death protein 10 (PDCD10) mRNA encodes a highly conserved scaffold protein, also known as CCM3, which is essential for vascular development and cellular homeostasis [1, 2]. PDCD10 functions as a core component of the Cerebral Cavernous Malformations (CCM) complex and the striatin-interacting phosphatase and kinase (STRIPAK) complex, regulating signaling pathways that maintain endothelial cell-cell junctions and Golgi apparatus organization [3]. Mutations in the PDCD10 gene are the primary cause of Cerebral Cavernous Malformations type 3, a condition characterized by fragile, leaky blood vessels in the brain that can lead to hemorrhage and seizures [4]. Beyond its vascular role, PDCD10 is involved in regulating apoptosis and cell proliferation, and its dysregulation is observed in various cancers, including glioblastoma and breast cancer [3]. As a therapeutic target, PDCD10 mRNA is being explored for modulation via antisense oligonucleotides and RNA interference to either restore vascular integrity or inhibit its pro-survival roles in oncology [5]. While no drugs targeting PDCD10 mRNA are currently FDA-approved, it remains a significant focus of research for treating both genetic vascular diseases and certain malignancies.
Antisense inhibition of mRNA translation and RNA interference-mediated degradation of PDCD10 transcripts.
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