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

GSE312326 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2026/02/27 Platform GPL24676
Summary
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.
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Also filed as BioProject PRJNA1373032 and SRA study SRP650983. Searching any of these in the dataset finder brings you back here.

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