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Recently, Luo et al. demonstrated that HIF could directly regulated mouse Snail expression [ 53].
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In a transgenic mouse model of breast cancer, Snail expression was associated with a more aggressive phenotype and poorer survival rates [ 6].
In a transgenic mouse model of breast cancer, Snail expression was associated with a more aggressive phenotype, higher risk of tumour recurrence, and with poor survival rates (Moody et al, 2005).
Pointing in the same direction are the data from conditional hypomorphic Snail expression in mice, in which resistance to radiation and to formation of spontaneous epithelial and mesenchymal tumors is increased [ 19].
This apparent discrepancy was initially ascribed to a swapping of Slug and Snail expression domains in the mouse [25], [26].
Expression of human E-cad, mouse Snail, and mouse SIP1-proteins was assessed by Western blot analysis.
Expressions of human E-cad, mouse Snail, and mouse SIP1 mRNA in the various clones were confirmed by RT PCR.
Ectopic expression of GLI1 induces the nuclear Snail expression and concomitant loss of E-cadherin expression in mouse mammary gland tissue during pregnancy [ 32].
Our previous work using a colitis-associated cancer model showed a trend towards smaller tumors in ILK-ko mice that, was accompanied by a reduction in both cyclin D and Snail expression.
The reduction in Snail expression, which has been linked to EMT [ 32], in our ILK-ko mice is also of interest as the FVB strain of mice are known to undergo more fibrosis [ 15], and this is attenuated in the ILK-ko mice.
Snail was widely expressed (96.1%) and 81.6% of the cases showed high Snail expression.
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