Ro52 expression increases the sensitivity of cells to TRAIL-induced apoptosis

摘要

TRAIL as a specific anticancer agent specifically induces apoptosis in a broad range of tumor cells while leaving normal nontransformed cells mostly unaffected. SSA/Ro52 is an autoantigen which presents in patients with Sjogren's syndrome (SS) and systemic lupus erythematosus (SLE). In the present study, we report that overexpression of Ro52 promotes cell apoptosis in response to TRAIL treatment by hastening the activation of caspase-3. This suggests that TRAIL treatment for patients with increased expression of Ro52 maybe appear side effect on Systemic autoimmune disease (SAID) via the increased apoptosis leading to autoantigenic exposure and generation of Ro52 autoantibodies, promoting autoreactivity.