Skip to main content
. 2018 Apr 24;9(31):21876–21892. doi: 10.18632/oncotarget.25082

Figure 3. SIK2 inhibits migration and invasion of breast cancer cell lines via blocking EMT.

Figure 3

The effect of SIK2 in the motility and invasiveness behavior of the breast cells was investigated in the cell lines with SIK2 modulation. (A) Effect of stable downregulation of SIK2 on the motility of MCF12A cells were evaluated relative to the control cells by wound healing assay. Cells migrated to the scratch area were counted at the indicated time points. (B) Potential changes in invasive characteristics of MCF12A cells upon stable SIK2 down-regulation were assessed by matrigel trans-well assay. Filters were collected at 48 hours after the initial seeding; cells were stained with Giemsa and counted. (C) Effect of stable upregulation of SIK2 on the migration of MDA-MB-231 cells was analyzed by RTCA analysis in a 24 hours’ time frame. (D) Effect of SIK2 downregulation on E-cadherin and MMP2 expression profiles of MCF12A cells was studied by Western blot analysis. (E) Efficacy of transient SIK2 silencing by siRNA in MCF12A cells was assessed by Western blotting and its impact on the expression of indicated EMT markers was compared to control cells (siAllStar) by qRT-PCR. (F) Effect of SIK2 upregulation on indicated EMT markers in MDA-MB-231 cells was evaluated by qRT-PCR. In Western blotting either anti-β-actin or anti-GAPDH antibody was used for loading control, HPRT and GAPDH were used as the internal controls in qRT-PCR. All experiments were done in triplicate. **P< 0.001, and *P≤ 0.05.