CYLD lysine 63 deubiquitinase mRNA (CYLD)

CYLD lysine 63 deubiquitinase (CYLD) mRNA encodes a critical deubiquitinating enzyme that serves as a potent tumor suppressor by negatively regulating the NF-kappaB and JNK signaling pathways (UniProt Q9NQC7). The encoded protein specifically cleaves Lys-63-linked polyubiquitin chains from key signaling adapters such as TRAF2, TRAF6, and NEMO, thereby preventing the constitutive activation of pro-inflammatory and pro-survival genes (PubMed: 12717450). Mutations in the CYLD gene or significant downregulation of its mRNA are the primary drivers of Brooke-Spiegler syndrome and are frequently observed in various malignancies, including skin, liver, and lung cancers, where the loss of CYLD promotes tumor progression and resistance to apoptosis (NCBI Gene ID: 1540). In the realm of drug development, CYLD mRNA is a target for innovative RNA-based therapies, particularly mRNA replacement strategies aimed at restoring its tumor-suppressive activity in deficient cells. While no drugs targeting CYLD mRNA are currently FDA-approved, its central role in controlling inflammation and cell survival makes it a high-priority target for both oncology and chronic inflammatory disease research.

Other names

Cylindromatosis (turban tumor syndrome)CYLDIEACMFTMFT1SBSTEMUSPL2Ubiquitin carboxyl-terminal hydrolase CYLD mRNA

Therapeutic approaches include mRNA replacement therapy to restore tumor suppressor function in deficient cells or the use of RNA interference (siRNA) and antisense oligonucleotides (ASOs) to modulate expression for research and potential immune-oncology applications.