Anti-antioxidant impacts of circZNF609 silence in HaCaT cells through regulating miR-145.

CircZNF609 (cZNF609) is previously revealed as an essential mediator in oxidative stress. This paper determined the role of cZNF609 in skin oxidative damage to evaluate its importance in pressure ulcer. HaCaT cells treated by HO were considered as a cell model of pressure ulcer. The role of cZNF609 in the model was checked by conducting CCK-8 assay, FITC-PI double-staining, ROS detection and Western blot. The downstream gene and signalling of cZNF609 were studied by utilizing qRT-PCR and Western blot. HaCaT cells were remarkably damaged by HO, as evidenced by the viability loss, apoptosis and ROS generation. It was coupled with the elevated expression of p53, p16, Bax and the activated forms of caspase-3 and PARP. Meanwhile, cZNF609 was high-expressed in response to HO. The oxidative stress driven by HO was alleviated by transfection with cZNF609 specific siRNA. Further, the anti-antioxidant impacts of cZNF609 silence were impeded by miR-145 silence. The inhibition of JNK and p38MAPK pathways induced by cZNF609 silence was impeded by miR-145 silence. The protective function of cZNF609 silence in HO-injured HaCaT cells was revealed . Silence of cZNF609 exhibited its impact possibly through regulating miR-145, and JNK and p38MAPK pathways.