Induction of Rad51 protein levels by p38 MAPK decreases cytotoxicity and mutagenicity in benzo[a]pyrene-exposed human lung cancer cells.

摘要: Rad51 is an essential component of the homologous recombination repair pathway. Abnormal expression has been reported in various carcinomas. Benzo[a]pyrene (B[a]P), a polycyclic hydrocarbon carcinogen found environment, induces cancer multiple organs. B[a]P shown to activate p38 MAPK signaling pathway mammalian cells. The prime purpose this study was determine how activates pathway, and then regulates human Exposure lung cells with increased protein levels time- dose-dependent fashion. also induced mRNA synthesis. Blockage activation by SB202190 or small interfering RNA (si-p38) decreased B[a]P-elicited increasing instability, but did not affect transcription. Furthermore, enhancement constitutively active MKK6 (MKK6E) stability. Moreover, B[a]P-induced cytotoxicity mutagenicity were significantly depleted endogenous Rad51. Taken together, these results indicate that provides critical role inhibiting B[a]P-treated work points unexpected control stability response exposure.