Fig. 2

Stathmin interferes with microtubule dynamics. aThere is a stathmin-microtubule-EMT (S-M-E) axis during cancer development; stathmin promotes malignant potential in cancer cells by initiating EMT; phosphoinositide 3-kinase (PI3 K)/mTOR/HSP90 are suggested as possible targets in p-stathmin(S38)-high cases; b siva1 enhances the formation of microtubules and impedes adhesion, cell migration, and EMT by inhibiting stathmin’s activity; inhibition of LMP1 expression attenuates the interaction of ERK with stathmin and promotes microtubule depolymerization; c induction of LRRC4 or knockdown of stathmin induces cell cycle arrest by modulating the p21, cyclin D1, and cyclin B expression, and the ERK phosphorylation. PI3 K phosphoinositide 3-kinase, mTOR mammalian target of rapamycin, HSP90, heat shock protein 90, EMT epithelial-mesenchymal transition, Siva proapoptotic protein, LMP1 latent membrane protein 1, ERK extracellular regulated protein kinases, RSK2 p90 ribosomal S6 kinase 2, LRRC4 leucine rich repeat containing 4, CDK5 cyclin-dependent kinase-5, CDC2 cyclin-dependent kinase 1, p21 cyclin-dependent kinases