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Centrosomal protein of 55 kDa (CEP55) mRNA encodes a critical scaffolding protein essential for the final stage of cell division known as abscission. During cytokinesis, the CEP55 protein localizes to the midbody where it recruits the endosomal sorting complex required for transport (ESCRT) machinery, specifically TSG101 and ALIX, to facilitate the physical separation of daughter cells [1][2]. While its expression is strictly regulated and typically low in most differentiated tissues, CEP55 mRNA is significantly overexpressed in a wide variety of human malignancies, including breast, lung, and liver cancers [3][4]. This overexpression drives uncontrolled cell proliferation, promotes genomic instability, and is strongly correlated with poor clinical prognosis and tumor aggressiveness [5]. Consequently, CEP55 mRNA has emerged as a promising therapeutic target, with experimental strategies utilizing small interfering RNAs (siRNAs) or antisense oligonucleotides (ASOs) to knockdown its expression, thereby inducing cell cycle arrest and apoptosis in cancer cells [6][7]. Beyond its role in oncology, mutations in the CEP55 gene are associated with Marchal-Chaud-Casati syndrome, a severe neurodevelopmental disorder characterized by microcephaly [1].
RNA interference (RNAi) or antisense-mediated degradation of mRNA leading to reduced protein expression and subsequent inhibition of cytokinesis and induction of apoptosis.
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