Fig. 6: Ln268 enhances stress inducers to inhibit cancer cell growth.
From: Developing novel Lin28 inhibitors by computer aided drug design
A, B DuNE cells were transfected with GFP-tagged Lin28b together with either RFP-tagged G3BP1, YB-1, or DCP1. Cells were then challenged with ARS (A), cisplatin (CP) or etoposide (etop) (B) to induce a stress condition. Confocal microscope detected the subcellular localization of Lin28b. C, D Du145, DuNE and DuNE(KO) cells were treated with ARS (C), cisplatin (CP) or etoposide (etop) (D). Percentage of cells forming SGs was counted in five random fields from two replicate experiments. E DuNE and DuNE(KO) cells were treated with ARS, cisplatin or etoposide. Cell viability was measured by Incucyte. F DuNE cells were transfected with GFP-tagged Lin28b and treated with ARS together with C1632, Ln15, Ln268, or RNase. Confocal microscope detected SGs formation mediated by Lin28b. Fluorescence images were captured, and SGs sizes and numbers were calculated as shown. G DuNE cells were co-treated with increasing concentrations of Ln268 plus cisplatin, etoposide and ARS. Drug interactions were calculated by SynergyFinder, with a synergy score higher than 10 representing synergistic relationship. Three independent biological replicates were performed for all the assays. All results are presented as the mean ± SD.
