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Fig. 3 | Journal of Translational Medicine

Fig. 3

From: Stathmin-dependent molecular targeting therapy for malignant tumor: the latest 5 years’ discoveries and developments

Fig. 3

Stathmin affects the proliferation of cancer cells. a Stathmin cooperates with p21(Cip1/Waf1) and p27(Kip) to control the early phase of G1 to S phase and reduces tumor growth by down-regulation of Nf-κB; b stathmin knockdown inhibits the expression of HIF-1α and VEGF and phosphorylation of S6 K and Akt; stathmin binds phosphorylation of p53(MUT) by DNA-PKCS, but inhibition of stathmin or DNA-PKCS results in M phase failure by impairing p53(MUT)-dependent transcription; c down-regulation of CREB1 and LYL1 reduces cell proliferation by the down-regulating stathmin; knockdown of stathmin promotes the effects of indoly-chalcones CITs; stathmin enhances growth and invasion of EC by activating MMP2 and MMP9; inhibition of Rlim increases expression of stathmin and leads to cell proliferation; inhibition of Aurora A by stathmin promoter inhibits cells proliferation by reducing expressions of phosphatidylinositol 3 kinase/Akt and p-BRCA1; stathmin potentiates cell proliferation by regulating function of p27. p21 cyclin-dependent kinases, p27 cell cycle checkpoints regulator protein, PI3 K phosphoinositide 3-kinase, Nf-κB nuclear factor ‘kappa-light-chain-enhancer’ of activated B-cells, Akt v-akt murine thymoma viral oncogene, S6 K ribosomal protein S6 kinase 1, HIF-1α hypoxia-inducible factor-1, VEGF vascular endothelial growth factor, p53 tumor suppressor p53, DNA-PKCS catalytic subunit of the DNA-dependent protein kinase, CREB1 leucine zipper transcription factor, LYL1 basic helix-loop-helix transcription factor, Rlim a Ring H2 zinc finger protein, MMP matrix metalloproteinases, p-BRCA1 phosphorylated phosphorylated breast cancer gene 1, CITs, indoly-chalcones

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