Fig. 5: GOLGA2P10 suppresses ER stress-induced apoptosis by increasing BCL-xL level. | Cell Death & Disease

Fig. 5: GOLGA2P10 suppresses ER stress-induced apoptosis by increasing BCL-xL level.

From: LncRNA GOLGA2P10 is induced by PERK/ATF4/CHOP signaling and protects tumor cells from ER stress-induced apoptosis by regulating Bcl-2 family members

Fig. 5

a, b GOLGA2P10 knockdown decreased BCL-xL protein level. Hepatoma cells transfected with the indicated RNA duplexes were incubated with DMSO (−) or tunicamycin (+) for 6–8 h (a) or without any treatment (b), followed by Western blotting. c Ectopic expression of GOLGA2P10 increased BCL-xL level. SK-HEP-1 cells with stable overexpression of GOLGA2P10 (P10) or control (Ctrl) vector were treated with DMSO (−) or tunicamycin (+) for 6 h, followed by Western blotting. d Ectopic expression of BCL-xL abrogated the pro-apoptosis effect of GOLGA2P10 silencing. SK-HEP-1 cells with stable overexpression of BCL-xL or control (Ctrl) vector were transfected with NC or siP10 for 24 h, then treated with DMSO (−) or tunicamycin (+) for 60 h, followed by DAPI staining or Western blotting. e Knockdown of BCL-xL abrogated the anti-apoptosis effect of GOLGA2P10. SK-HEP-1 cells with stable overexpression of GOLGA2P10 (P10) or control (Ctrl) vector were transfected with NC or siBCL-xL for 24 h, then treated with DMSO (−) or tunicamycin (+) for 48 h, followed by DAPI staining. − absence, + presence. β-actin was used as an internal control. For DAPI staining analyses in (d, e), data are shown as mean ± SEM of three independent experiments. For Western blotting in a–d, two independent experiments were performed with similar results. *P < 0.05; ***P < 0.001; ns not significant.

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