MiR-205 reduces epithelial-mesenchymal transition(EMT) through regulating zinc finger E-box binding homeobox2 (ZEB2) expression. Knockdown of miR-205 by transfection with 50 nM anti-miR-205 inhibitor significantly increased the invaded cell numbers on the Matrigel invasion assay as described in Materials and Methods, while overexpression of miR-205 by 50 nM miR-205 precursor transfection significantly inhibited the transmembrane ability compared to control scramble oligonucleotides (A). Transfection with 50 nM miR-205 precursor significantly inhibited the distance of OE21 cell migration, while transfection with 50 nM anti-miR-205 inhibitor tended to promote in vitro wound healing as described in Materials and Methods, though it is not significant (B). Western blot showed that knockdown of miR-205 by 50 nM anti-miR-205 inhibitor transfection leaded to enhanced expression of zinc finger E-box binding homeobox (ZEB) 2 but not ZEB1 in OE21 cells (C). The downregulation of miR-205 decreased cellular E-cadherin expression, and instead, N-cadherin appeared in the OE21 cells transfected with anti-miR-205 inhibitor. Overexpression of miR-205 by its precursor (50 nM) did not affect the expression levels of ZEBs and E- and N-cadherin. Transfection of anti-miR-205 inhibitor but not miR-205 precursor reduced cellular expression of phospho-Akt (C).
Matsushima et al. Journal of Translational Medicine 2011 9:30 doi:10.1186/1479-5876-9-30