Figure 7. TGFβ2 is a critical mediator of miR-191 induced breast cancer migration under hypoxia.

(a, b). Effect of miR-191 and TGFβ2 on migration under hypoxia. (a, b) The cells were transfected with control miRNA or miR-191mimic along with TGFβ2 silencing using esiTGFβ2 and migration was quantitated using Boyden chamber assay (a) or wound healing assay (b). The results from the three cell lines show that miR-191 mediated increase in migration is abolished with the TGFβ2 silencing. (c, d) The cells were transfected with control miRNA or anti-miR-191 along with TGFβ2 overexpression and migration was quantitated using Boyden chamber assay (c) or wound healing assay (d). The results show that the decrease in migration by inhibition of miR-191 was reduced when TGFβ2 was coexpressed. (e). miR-191 induced migration is SMAD3 dependent as reduction in migration was observed on miR-191 overexpression along with the inhibition of SMAD3. (f). A proposed model detailing hypoxic regulation of miR-191 along with its functional impact on HIF & TGFβ-pathways and further implication in regulation of migration of hypoxic breast cancer. The graphical data points in a-e represent mean ± S.D of at least three independent experiments. (*P < 0.05, **P < 0.01). Error bars denote ± SD.