MiR-20b-5p Is Involved in Hydroquinone-Induced TK6 Cell Cycle Arrest and Oxidative Damage Through JNK1 Signaling Pathway and Targeting Nrf2.

Hydroquinone (HQ), a metabolic byproduct of benzene, can cause oxidative damage. Oxidative stress triggers the excessive generation of reactive oxygen species (ROS), which in turn elicits diverse forms of cellular injury, including cell cycle arrest. This study sought to investigate the role and underlying regulatory mechanism of miR-20b-5p in HQ-induced cellular injury. The findings indicated that HQ increased the proportion of S-phase cells, indicating S-phase arrest. Furthermore, miR-20b-5p deletion facilitated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream proteins, while also stimulating the expression of downstream proteins associated with c-Jun N-terminal kinase 1 (JNK1). Therefore, we speculate that loss of miR-20b-5p exacerbates HQ-induced cytotoxicity and S-phase cell accumulation, potentially through the JNK1/Nrf2 signaling pathway or via direct regulation of Nrf2.