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DKC1 promotes colorectal cancer progression and therapy resistance by dysregulating sphingolipid biosynthesis

ABSTRACT: Higher expression of Dyskerin Pseudouridine Synthase 1 (DKC1) associates with poor prognosis in colorectal cancer (CRC) patients. However, the mechanism associated with DKC1 upregulation, and its functional significance in disease pathogenesis and therapeutic resistance remains largely unexplored. Here, we performed global transcriptome sequencing outlining the molecular mechanism associated with DKC1 depletion in CRC. We show a positive feedback loop between canonical WNT signaling and DKC1, which orchestrates DKC1 expression. Moreover, we show the role of altered sphingolipid metabolism upon DKC1 abrogation in imparting CRC oncogenicity and first-line chemotherapeutic resistance.

ORGANISM(S): Homo sapiens

PROVIDER: GSE312326 | GEO | 2026/02/27

REPOSITORIES: GEO

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Genome-wide RNAi Screening Identifies pseudouridine synthase DKC1 promotes CRC proliferation through regulating ribosomal proteins expression

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