ANLN plays a critical role in human lung carcinogenesis through the activation of RHOA and by involvement in the phosphoinositide 3-kinase/AKT pathway.

摘要: Gene expression profile analysis of non-small cell lung cancers (NSCLC) and subsequent functional analyses revealed that human ANLN, a homologue anillin, an actin-binding protein in Drosophila, was transactivated cancer cells seemed to play significant role pulmonary carcinogenesis. Induction small interfering RNAs against ANLN NSCLC suppressed its resulted growth suppression; moreover, treatment with RNA yielded larger morphology multiple nuclei, which subsequently died. On the other hand, induction exogenous enhanced migrating ability mammalian by interacting RHOA, guanosine triphosphatase, inducing actin stress fibers. Interestingly, inhibition phosphoinositide 3-kinase/AKT activity decreased stability caused reduction nuclear level. Immunohistochemical staining on tissue microarrays associated poor survival patients, indicating this molecule might serve as prognostic indicator. Our data imply up-regulation is common feature carcinogenetic process tissue, suggests selective suppression could be promising approach for developing new strategy treat cancers.