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Fig. 4 | BMC Cancer

Fig. 4

From: The Aplidin analogs PM01215 and PM02781 inhibit angiogenesis in vitro and in vivo

Fig. 4

Aplidin analogs induce premature senescence by induction of the cell cycle inhibitor p16INK4A. a HUVECs (n = 3) were stimulated for 24 h with the compounds, after which total RNA and protein was extracted. Gene expression was analyzed by real-time PCR and protein expression by SDS-PAGE and Western Blot. Aplidin™ (5 nM) and Aplidin derivatives (10 nM) induced p16INK4A gene expression. TP53 gene expression was induced neither by bortezomib (5 nM) nor by Aplidin (5 nM) or derivatives (10 nM). P27KIP1 gene expression was induced only by bortezomib. b Western Blot analysis of p16INK4A protein after treatment with bortezomib, Aplidin™ and derivatives (72 h). c Upregulation of p53 and cell cycle inhibitors p21 and p27 after treatment with the proteasome inhibitor bortezomib (24 h). Aplidin™ and derivatives did not induce p53, p21 or p27 proteins, even after 72 h of incubation (data not shown). Tubulin alpha served as loading control. d Staining for senescence-associated beta galactosidase in human endothelial cells treated for 72 h with Aplidin™ (5 nM) and analogs (10 nM each). In comparison to control Aplidin analog-treated cells show an increased number of blue (SA-β- gal positive) cells, like the positive control H2O2. Differences between the means of one treatment group and untreated control were analyzed. The level of significance for the analysis was set at p < 0.05. Bars indicate 20 μm

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