Fig. 4

Stathmin correlates with apoptosis and mobility of cancer cells. a Oxidative stress induces JNK-dependent stathmin phosphorylation, but down-regulation of stathmin promotes apoptosis of cells and inhibits proliferation and migration; stathmin silencing with paclitaxel enhances tumor cell apoptosis; JAK2(V617F) mutation potentially leads to inhibition of stathmin activity via STAT3 phosphorylation; b silencing of stathmin increases apoptosis of cells by down-regulating Bcl-2 and survivin and activating Caspase-3, and significantly arrests the cell cycle at G2/M phase; c stathmin attributes to E2F1 and/or Dp-1 (TFDP1) transactivation, knockdown of the E2F1 suppresses cancer cell migration; stathmin counteracts PDEF’s effects against cell migration; d SIVA silencing increases cell migration by promoting stathmin activity, but ANKHD1 silencing leads to stathmin inactivation likely through inhibition of SIVA/stathmin association; MCPyV tumor antigen promotes the destabilization of the host cell microtubule network by regulating phosphorylation of stathmin, which leads to migratory cell phenotype. JNK c-JunN-terminalkinase, JAK janus kinase, JAK janus kinase, STAT signal transducers and activators of transcription, Bcl-2 B cell lymphoma-2, E2F1 E2F transcription factor 1, TFDP1 transcription factor Dp-1, PDEF prostate-derived Ets transcription factor, SIVA proapoptotic protein, ANKHD1 ankyrin repeat and KH domain containing 1 protein, MCPyV Merkel cell polyomavirus