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. 2014 May 30;19(6):7122–7137. doi: 10.3390/molecules19067122

Figure 6.

Figure 6

miR-221 and miR-222 suppressed expression of SOCS1 and CDKN1B. (A) Schematic representation of the Human SOCS1 3' UTR showing the highly conserved miR-221/222 binding site (highlighted and boxed) between species. The “seed” sequence of miR-221/222 (nt 2–7) is complementary to the SOCS1 3' UTR. (B) Sequence analysis of the 3' UTR of CDKN1B mRNA identified two conserved binding sites to the “seed” sequence of miR-221 and miR-222. (C) Western blot analysis indicating the inhibition of SOCS1 expression by miR-221/222 overexpression in MCF-7 cells. β-actin served as loading control. (D) Western blot analysis indicating the up-regulation of SOCS1 by miR-221/222 inhibitors in MDA-MB-231 cells. miR-155 was used as positive control for targeting SOCS1. β-actin served as loading control. (E) Western blot analysis demonstrating the up-regulation of CDKN1B by miR-221/222 inhibitors in MDA-MB-231 cells. β-tubulin served as loading control. (F) SOCS1 overexpression in MDA-MB-231 cells suppressed cellular migration. Data are mean ± SEM (n = 3). ** p < 0.01.