Fig. 6: Nimbolide modulates PI3K/Akt/GSK-3β via targeting HOTAIR and miR-126. | Cell Death & Disease

Fig. 6: Nimbolide modulates PI3K/Akt/GSK-3β via targeting HOTAIR and miR-126.

From: Nimbolide, a neem limonoid inhibits cytoprotective autophagy to activate apoptosis via modulation of the PI3K/Akt/GSK-3β signalling pathway in oral cancer

Fig. 6

a Western blots showing expression of phosphorylated and unphosphorylated GSK-3β in cells treated with nimbolide for 0 to 96 h. Gapdh was used as loading control. b Immunoblot analysis of PI3K, p-AktSer473, and Akt in cells treated with nimbolide for 0 to 96 h. Gapdh was used as loading control. c Immunoblot analysis of molecules involved in autophagy in SCC4 cells transfected with empty plasmid and PI3K plasmid in the absence or presence of nimbolide. Gapdh was used as loading control. d Immunoblot analyses of Bax, Bcl-2, cytochrome c, cleaved caspase-9 and -3 in empty plasmid and PI3K plasmid transfected cells in the absence or presence of nimbolide.The data presented are representative of three independent experiments. e qRT-PCR analysis of miR-126 and HOTAIR in SCC131 and SCC4 cells. Data are the mean ± SD of three independent experiments. f Transcript expression level of miR-126 and GSK-3β in control and miR-126 overexpressed cells in the presence or absence of nimbolide (6 µm) as determined by quantitative RT-PCR. ♣ Significantly different from control (p < 0.001)

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