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Gramantieri L et al. – The results indicate that miR–221, by targeting Bmf, inhibits apoptosis. Moreover, in HCC, miR–221 overexpression is associated with a more aggressive phenotype. These findings, together with the previously reported modulation of CDKN1B/p27 and CDKN1C/p57, show that miR–221 simultaneously affects multiple pro–oncogenic pathways and suggest miR–221 as a potential target for nonconventional treatment against HCC.



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