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Inactivating CUX1 mutations promote tumorigenesis.

Chi C Wong1, Inigo Martincorena2, Alistair G Rust3

  • 11] Experimental Cancer Genetics, Wellcome Trust Sanger Institute, Hinxton, Cambridge, UK. [2] Department of Haematology, University of Cambridge, Hills Road, Cambridge, UK.

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The homeodomain transcription factor gene CUX1 (cut-like homeobox 1) acts as a tumor suppressor. Inactivating mutations in CUX1 drive various cancers by activating PI3K signaling, offering a new therapeutic target.

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Area of Science:

  • Oncology
  • Cancer Genetics
  • Molecular Biology

Background:

  • Identifying cancer-driving mutations is crucial for effective treatment.
  • Low-frequency somatic mutations in cancer genetics pose a significant challenge.
  • The role of the CUX1 gene in tumorigenesis requires further investigation.

Purpose of the Study:

  • To investigate the role of the CUX1 gene in human cancers.
  • To determine if CUX1 mutations are drivers of tumorigenesis.
  • To explore therapeutic strategies for CUX1-mutant tumors.

Main Methods:

  • Genomic interrogation of 7,651 diverse human cancers.
  • Meta-analysis of CUX1 mutational status in 2,519 myeloid malignancies.
  • Validation using mouse transposon-mediated insertional mutagenesis and Drosophila cancer models.

Main Results:

  • Inactivating mutations in CUX1 were identified in ~1-5% of various human tumors.
  • Disruptive CUX1 mutations in myeloid malignancies were associated with poor survival.
  • CUX1 deficiency was shown to activate phosphoinositide 3-kinase (PI3K) signaling by downregulating PIK3IP1.

Conclusions:

  • CUX1 functions as a bona fide tumor suppressor gene.
  • CUX1 mutations are pan-drivers of tumorigenesis across diverse cancer types.
  • Targeting PI3K-AKT signaling presents a potential therapeutic strategy for CUX1-mutant cancers.