Fig. 6: ALDH7A1 overexpression promotes glycolysis of heat-induced HCC cells and protects the cells against hyperosmotic stress. | Cell Death Discovery

Fig. 6: ALDH7A1 overexpression promotes glycolysis of heat-induced HCC cells and protects the cells against hyperosmotic stress.

From: Tanshinone IIA inhibits heat-induced growth of p53-mutant Huh-7 hepatocellular carcinoma by modulating osmotic homeostasis and glycolysis through targeting ALDH7A1

Fig. 6

A–C Validation of ALDH7A1 OE at mRNA and protein levels using qPCR and western blotting. ALDH7A1 OE promotes glucose uptake (D), lactate production (E), and ATP level F in the heated HCC cells. ALDH7A1 OE increases the levels of its enzymatic and/or osmolytic products NADH (G), betaine (H) and d-glycerate (I). J, K ALDH7A1 OE enhances its downstream ROS but does not influence lipid peroxidation. In (A–K), *p < 0.05, **p < 0.01, compared with EV (empty vector) group. L Hyperosmotic stress inhibits the viability of the cells with or without ALDH7A1 OE, and ALDH7A1 OE enhances the viability of heat-induced HCC cells in hyperosmotic culture media. M, N ALDH7A1 OE does not significantly inhibit hyperosmotic stress-induced apoptosis of HCC cells pretreated with heat. O–R ALDH7A1 OE promotes invasion and EMT of the heat-induced HCC cells under hyperosmotic stress. Iso, isosmotic; Hyper, Hyperosmotic. In (L–R), *p < 0.05, **p < 0.01, compared with EV+Iso group; # p < 0.05, ## p < 0.01, compared with ALDH7A1-OE+Iso group; + p < 0.05, ++ p < 0.01, compared with EV+Hyper/NaCl or EV+Hyper/Glucose group.

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