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. 2017 Jul 14;7:5376. doi: 10.1038/s41598-017-05512-9

Figure 3.

Figure 3

AE-AS decreased HIF-1α protein degradation and synthesis, and WSB-1-pVHL interaction in hypoxic T24 cells. T24 cells were exposed to hypoxia for 8 h followed by addition of cycloheximide (CHX, 10 μg/ml) in the presence or absence of AE-AS (40 μg/ml) for different time periods. The HIF-1α protein levels at indicated time were analyzed (A). In the presence of proteasome inhibitor MG132 (10 μM) and hypoxia, the interaction of pVHL and HIF-1α in various groups was examined (B). The T24 cells were pretreated with MG-132 for 1 h followed by exposure of hypoxia for 8 h in the presence or absence of AE-AS, and the HIF-1α protein levels were determined (C). Data was expressed as mean ± SEM (n = 5). *P < 0.05 versus hypoxia and MG132-treated alone cells. The nuclear protein level of HIF-1α and VEGF synthesis in the presence or absence of si-WSB-1 in hypoxic T24 cells were analyzed (D). The expression of WSB-1 and pVHL (E), and the association of WSB-1 with pVHL (F) in various groups were determined. *P < 0.05, ***P < 0.001 versus normoxic cells; ## P < 0.01 versus hypoxia-treated alone cells.