Abstract
BCC or not: Sufu keeps it in check.
Highlights
Basal cell carcinoma (BCC), driven by aberrantly activated HEDGEHOG (HH) pathway, is the most common human malignancy
We have previously shown that loss of Sufu in mouse keratinocytes promotes Gli2 nuclear localization due to lack of cytoplasmic sequestration, and leads to elevated target gene expression[3]
These results indicate that Ptch1 knockout cells are able to override the checkpoint and continue proliferation with the unstable genome while Sufu knockouts halt, a key feature likely contributing to their differential cancer phenotypes
Summary
Basal cell carcinoma (BCC), driven by aberrantly activated HEDGEHOG (HH) pathway, is the most common human malignancy. Upon HH binding, SMO promotes dissociation of GLI transcription factors from the key negative intracellular regulator SUFU, thereby allowing expression of HH target genes[2]. Mutations in PTCH1, SMO, and SUFU, believed to unleash GLI activity, are frequently found in BCC.
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