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Fig. 4 | Cancer Cell International

Fig. 4

From: SGLT2 inhibition restrains thyroid cancer growth via G1/S phase transition arrest and apoptosis mediated by DNA damage response signaling pathways

Fig. 4

The effect of canagliflozin on DNA damage response and apoptosis in thyroid cancer. A Canagliflozin induced γ-H2AX expression in TPC-1 and BCPAP cells. TPC-1 and BCPAP cells were treated with 0, 10, 20 μM canagliflozin for 24 h, and γ-H2AX expression levels were detected by western blot. GAPDH was used as a loading control. One-way ANOVA were used to determine statistical significances. B Canagliflozin increased the phosphorylation of ATM and CHK2 in TPC-1 and BCPAP cells. TPC-1 and BCPAP cells were treated with 10 μM canagliflozin for 24 h, and the p-ATM and p-CHK2 were detected by western blot. GAPDH was used as a loading control. C Knockdown of SGLT2 increased p-ATM and p-CHK2 expression levels both in TPC-1 and BCPAP cells. 48 h after transfection, the cells were collected and analyzed by western blot. GAPDH was used as a loading control. D, E Canagliflozin induced ROS accumulation in TPC-1 and BCPAP cells. TPC-1 and BCPAP cells were treated 10 μM canagliflozin for 24 h, and cells were stained with DCFH-DA following flow cytometer analysis. A t-TEST was used to determine statistical significances. F, G Canagliflozin promoted cell apoptosis of TPC-1 and BCPAP cells. TPC-1 and BCPAP cells were treated 10 μM canagliflozin for 24 h, and cells were stained with Annexin V and PI following flow cytometer analysis. H Gene signatures for cell apoptosis were enriched in a subgroup treated with canagliflozin

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