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. 2019 May 10;44:361–374. doi: 10.1016/j.ebiom.2019.05.008

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This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 5 — Bestatin inhibits anchorage-independent growth and proliferation of colon cancer cells. (a) DLD-1 or HCT-15 colon cancer cells were treated with different concentrations of bestatin for 0, 24, 48, or 72 h and proliferation was estimated by a crystal violet staining assay. The data are shown as mean values ± S.E. from triplicate experiments. The asterisks (*, **) indicate a significant (p < .05, p < .01, respectively) decrease in proliferation compared to the vehicle-treated control group. (b) DLD-1 or HCT-15 colon cancer cells were treated with increasing doses of bestatin. The data are shown as mean values ± S.E. from triplicate experiments. The asterisks (*, **, ***) indicate a significant (p < .05, p < .01, p < .001, respectively) decrease in colony formation compared to the vehicle-treated control group. (c) DLD-1 or HCT-15 colon cancer cells were treated with different concentrations of bestatin. Cells were harvested and the expression levels of phosphorylated and total proteins were analyzed by Western blotting. (d) The schematic mechanism of bestatin's effects against colon cancer mediated through the LTA4H-BLT1-ERK1/2 pathway is illustrated. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)