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Resolution: standard / high Figure 4.
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 |