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Fig. 1 | BMC Cancer

Fig. 1

From: Shikonin derivatives cause apoptosis and cell cycle arrest in human chondrosarcoma cells via death receptors and MAPK regulation

Fig. 1

Influence of shikonin derivatives on chondrosarcoma viability and cell cycle distribution. a Chemical structures of shikonin (S), acetylshikonin (AS), and cyclopropylshikonin (CS); b Cell growth of two chondrosarcoma cell lines was inhibited in a dose-dependent manner by shikonin derivatives (mean ± SD, n = 6, measured in biological quadruplicates). c The statistical evaluation of cell cycle distribution after treatment with the IC50 concentrations of shikonin derivatives is shown in stacked bar charts. Cell populations in G0/G1, S, and G2/M phases are given as percentage of total cells (mean of n = 3). Treatment caused a dose dependent significant decrease in the number of cells in G0/G1 phase (black) and S phase (light grey), which was accompanied by a pronounced increase of cells in G2/M phase (dark grey). d Representative flow cytometry cell cycle measurements 24 h after treatment with shikonin. e Relative gene expression of the cell cycle regulator cdc25c after treatment with shikonin for 24 h revealed a highly significant reduction in SW-1353 (light grey striped) and Cal78 (dark grey dotted) cells (mean ± SD, n = 6, measured in triplicates). Statistical significances are defined as follows: * p < 0.05; ** p < 0.01; *** p < 0.001

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