The SNAIL and SLUG transcription factors play important roles in embryogenesis owing to their anti-apoptotic properties and their ability to promote morphogenetic changes by inducing epithelial-mesenchymal transitions (EMT). These characteristics provide many of the proteins in these families with oncogenic and pro-metastatic capabilities when reactivated in cancers. The SCRATCH subgroup of the SNAIL superfamily, including SCRATCH1 and SCRATCH2, display distinct embryonic functions and diverge early in evolution. Despite the described overexpression of SCRT1 (encoding for SCRATCH1) in a small subset of human lung cancers, there is little data supporting a role of SCRATCH proteins in tumorigenesis. To further explore this possibility, we assessed SNAI1 (SNAIL), SNAI2 (SLUG) and SCRT1 (SCRATCH1) expression in a wide panel of human and murine tumors encompassing 151 primary tumors and 6 different cancer types, including melanomas and multiple different carcinomas. Whereas SNAI1 and SNAI2 are widely expressed in human and murine tumors, our results reveal that SCRT1 transcripts are undetectable in nearly all of the examined tumors sug-gesting that SCRATCH1 plays a minor role, if any, in tumorigenesis. Our data therefore suggest that oncogenic properties are not shared by all SNAIL superfamily members but instead are specifically allotted to the SNAIL subgroup supporting the conclusions that SNAIL and SCRATCH subgroups are functionally divergent and strengthening the hypothesis that the oncogenic potential of SNAIL and SLUG proteins relies on the hijacking of their embryonic functions.

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