Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Lunatic fringe deficiency cooperates with the Met/Caveolin amplicon to induce basal-like breast cancer

ABSTRACT: Mammary specific deletion of Lfng induces basal-like and claudin-low tumors with accumulation of Notch intracellular domain fragments, increased expression of proliferation-associated Notch targets, amplification of the Met/Caveolin locus, and elevated Met and Igf-1R signaling. Tumor DNAs from Lfngflox/flox; MMTV-Cre conditional mutant mice are being compared to control DNAs from the same animals in order to identify common alterations associated with tumor progression

ORGANISM(S): Mus musculus

SUBMITTER: Sean Egan 

PROVIDER: E-GEOD-35855 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Basal-like breast cancers (BLBC) express a luminal progenitor gene signature. Notch receptor signaling promotes luminal cell fate specification in the mammary gland, while suppressing stem cell self-renewal. Here we show that deletion of Lfng, a sugar transferase that prevents Notch activation by Jagged ligands, enhances stem/progenitor cell proliferation. Mammary-specific deletion of Lfng induces basal-like and claudin-low tumors with accumulation of Notch intracellular domain fragments, increa  ...[more]

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