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co-ordinated network of interaction in the signalling by these ligands functions and
mutual regulation of phenotypic outcome has been encountered in developing sys-
tems as well as in the activation of EMT, cell proliferation and tumour progression.
Therefore, targeting MTA3 signalling to modulate Wnt/E-cadherin pathway could
provide a potentially powerful means to inhibit EMT.
As noted earlier, both the short and long forms of MTA1 possess the potential to
modulate ER signalling. E-cadherin has been identified as the downstream target of
MTA signalling mediated by ER/E-cadherin via the transcription factor Snail which
regulates E-cadherin expression. As also noted above and illustrated in Figure 4.3,
the Wnt/E-cadherin pathway also involves regulation by Snail. Certain miRNAs have
been found to regulate EMT activation and preliminary studies do show that miR-
NAs might also regulate MTA expression. So MTAs might provide an alternative
albeit complex approach to cancer treatment, especially to TNBC management.
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