TIS21 modulates premature senescence via ROS-actin-linked cascade
Choi, Jung-A; Kim, Eun-Young; Lim, In Kyoung
Department of Biochemistry & Molecular Biology
Cellular senescence is a crucial anticancer mechanism that prevents cell growth at risk for neoplastic tranformtion. Recently, however, drug-induced senescence has been considered as promoting cancer progression to aggressive behavior. In this study, we observed that overexpression of TIS21, an antiproliferation gene, induced suppression of doxorubicin-induced senescence in Huh-7, human hapatoma cells. Generation of ROS (reactive oxygen species), which mediates cellular senescence, initiated by treatment of cells with doxorubicin was attenuated by overexpression of TIS21. Noticeably, doxorubincin-induced senescence developed alterations of F-actin and vimentin as the long and dense networks. In addition, Zyxin, a regulator of actin filament assembly, was rapidly mobilized from cytoplasm into nucleus. The changes mediated by doxorubicin might change the intracellular distribution and localization of actin-remodeling-associated proteins in addition to cytoskeletal proteins. These patterns changed by doxorubicin were able to be blocked by TIS21 and antioxidant, N-acetylcysteine, treatment. Taken together, the data suggest that overexpression of TIS21 inhibits doxorubicin-induced premature senescence via ROS-actin-associated protein cascades.
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