Fig. 5: ALKBH5 enhances PIK3R1 RNA stability in an m6A-YTHDF3-dependent manner and inhibits glycolysis. | Cell Death & Disease

Fig. 5: ALKBH5 enhances PIK3R1 RNA stability in an m6A-YTHDF3-dependent manner and inhibits glycolysis.

From: The dual mechanism of m6A demethylase ALKBH5 in regulating energy metabolism during exposure to MC-LR

Fig. 5

A PIK3R1 mRNA m6A methylation was increased upon knockdown of ALKBH5. B PIK3R1 mRNA m6A methylation was increased upon MC-LR exposure, which could be rescued by overexpressing ALKBH5. C YTHDF3 knockdown increased PIK3R1 mRNA expression. D YTHDF3 knockdown can reverse the change in PIK3R1 mRNA expression induced by ALKBH5 knockdown. E The half-life of PIK3R1 mRNA was shortened by ALKBH5 knockdown in THLE-3 cells. F The half-life of PIK3R1 mRNA was shortened upon MC-LR exposure, which could be rescued by overexpression of ALKBH5. G Effects of overexpression of ALKBH5 or simultaneous knockdown of PIK3R1 on cell proliferation inhibition induced by MC-LR exposure. Intracellular ATP levels (H), extracellular lactate production (I) and glucose uptake (J) were measured in PIK3R1 knockdown cells compared to control cells. Effects of ALKBH5 overexpression or PIK3R1 knockdown on intracellular ATP levels (K) and extracellular lactate production (L) in cells exposed to MC-LR. In THLE-3 (M) and THLE-2 (N) cells, ALKBH5 knockdown reduced the activity of PIK3R1’s WT. The A1557C mutation of PIK3R1 resulted in increased activity and was not affected by ALKBH5 knockdown. Data are means ± SD from three independent experiments. *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001.

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