Programmed cell death protein 10 (PDCD10) (PDCD10)

Programmed cell death protein 10 (PDCD10), also known as CCM3, is a highly conserved adaptor protein that plays a pivotal role in vascular development and cellular homeostasis [1, 3]. It functions as a core component of the Striatin-interacting phosphatase and kinase (STRIPAK) complex, which integrates signals to regulate diverse biological processes such as apoptosis, cell proliferation, and the structural organization of the Golgi apparatus [4]. Mutations in the PDCD10 gene are a primary cause of Cerebral Cavernous Malformations type 3 (CCM3), a severe vascular pathology characterized by the formation of leaky, dilated capillary lesions in the brain that can lead to intracranial hemorrhage and neurological deficits [5]. Beyond its role in vascular disease, PDCD10 is frequently overexpressed in various cancers, including glioblastoma and breast carcinoma, where it contributes to tumor cell survival, migration, and resistance to therapy [3]. Although no direct small-molecule inhibitors of the PDCD10 protein are currently approved, therapeutic research focuses on modulating downstream signaling pathways, such as the Rho-kinase (ROCK) pathway, or utilizing RNA-targeted therapies like antisense oligonucleotides to reduce its expression in oncogenic contexts [6, 8].

Other names

CCM3TFAR15Cerebral cavernous malformations 3 proteinProgrammed cell death protein 10 mRNA

Therapeutic approaches involve Rho-kinase (ROCK) inhibition to counteract the effects of PDCD10 loss in vascular disease, or RNA interference and antisense oligonucleotides to knock down PDCD10 mRNA in cancer contexts.