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. 2016 May 2;7(23):35257–35269. doi: 10.18632/oncotarget.9135

Figure 5. Knockdown of miR-592 enhances glycolysis by increasing WSB1-induced HIF-1α stability.

Figure 5

A. Western blot shows expression of HIF-1α, HIF-2α, c-Myc in HCC tissue and normal control (left panel). Quantitative RT-PCR shows the expression levels of HIF-1α mRNA in HCC tissue and normal control (right panel). B. The protein level of HIF-1α in SK-Hep-1 cells with overexpression or knockdown of WSB1 (left panel); mRNA level of HIF-1α in HCC cells with overexpression or knockdown of WSB1 (right panel). C. Expression of glycolysis-associated proteins (HK2 and Glut1) in HCC cells treated with the HIF-1α inhibitor YC-1 or overexpression of WSB1 (left panel); lactate production in the same cells (right panel). D. The protein level (left panel) or mRNA level (right panel) of HIF-1α with overexpression or knockdown of miR-592. E. The expression of HK2 and Glut1 in SK-Hep-1 cells treated with YC-1 and/or miR-592 knockdown (left panel); lactate production in HCC (right panel). F. The effect of CoCl2 on the expression of HK2 and Glut1 (left panel), and the effects of CoCl2 on lactate production (right panel) in SK-Hep-1 cells with WSB1 knockdown or miR-592 overexpression. The mean and SD of three independent experiments performed in triplicate are shown.