AI Article Synopsis
- SNAIL is a crucial transcriptional regulator that plays significant roles in embryonic development and cancer, specifically through its influence on epithelial-to-mesenchymal transition (EMT).
- Research indicates that SNAIL has oncogenic functions independent of EMT, exhibiting varied effects depending on the tissue and genetic context, such as either protecting against or promoting tumor growth in different types of cancer.
- The findings reveal that SNAIL's oncogenic effects do not involve typical mechanisms like E-cadherin downregulation, but instead facilitate cancer progression by bypassing cellular senescence and affecting cell cycle regulation through inactivation of the Retinoblastoma (RB) protein.
Article Abstract
SNAIL is a key transcriptional regulator in embryonic development and cancer. Its effects in physiology and disease are believed to be linked to its role as a master regulator of epithelial-to-mesenchymal transition (EMT). Here, we report EMT-independent oncogenic SNAIL functions in cancer. Using genetic models, we systematically interrogated SNAIL effects in various oncogenic backgrounds and tissue types. SNAIL-related phenotypes displayed remarkable tissue- and genetic context-dependencies, ranging from protective effects as observed in KRAS- or WNT-driven intestinal cancers, to dramatic acceleration of tumorigenesis, as shown in KRAS-induced pancreatic cancer. Unexpectedly, SNAIL-driven oncogenesis was not associated with E-cadherin downregulation or induction of an overt EMT program. Instead, we show that SNAIL induces bypass of senescence and cell cycle progression through p16-independent inactivation of the Retinoblastoma (RB)-restriction checkpoint. Collectively, our work identifies non-canonical EMT-independent functions of SNAIL and unravel its complex context-dependent role in cancer.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9992512 | PMC |
| http://dx.doi.org/10.1038/s41467-023-36505-0 | DOI Listing |
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