Stathmin Regulates Hypoxia-Inducible Factor-1 Expression through the Mammalian Target of Rapamycin Pathway in Ovarian Clear Cell Adenocarcinoma
Figure 3
Effects of PI3K inhibitor ((a) and (b)) and stathmin knockdown (c) on hypoxia-induced HIF-1α and VEGF expression in OVCAR-3 cells. ((a) and (b)) Cells were pretreated without (–) or with (+) a PI3K inhibitor, wortmannin (100 nM), for 30 min and then cultured under hypoxic conditions for 5 h. Cell lysates and total RNAs were subjected to immunoblot analysis (a, HIF-1α, HIF-1β, and β-actin) and semiquantitative RT-PCR analysis (b, VEGF and HIF-1α), respectively. Representative data from three independent experiments are shown. (c) Cells were treated with control (–), or stathmin (+) RNAi and then cultured under normoxic or hypoxic conditions for 5 h. Cell lysates were subjected to immunoblot analysis for phosphorylated p-Akt (p-Akt), total Akt (Akt), or HIF-1α. Representative data from three independent experiments are shown.
