Figure 4. miR-148a inhibited the protein expression of HIF-1α and Mcl-1 by directly targeting Met in the HT29 cell line under hypoxia. We created a hypoxic condition by using CoCl2 and evaluated the expression levels of HIF-1α and Mcl-1 in four cell lines (HT29, HT29 + bevacizumab, HT29-miR-148a, and HT29-miR-148a + bevacizumab). β-Actin served as an internal control. (A) Protein levels of Met, HIF-1α, and Mcl-1; (B) The Met protein expression level was significantly decreased in HT29-miR-148a cells but not in HT29 cells (P < 0.001); (C) The HIF-1α protein expression level was significantly decreased (P < 0.001). (D) The Mcl-1 protein expression level was markedly decreased (P < 0.001).