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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

From: Phenotype plasticity rather than repopulation from CD90/CK14+ cancer stem cells leads to cisplatin resistance of urothelial carcinoma cell lines

Fig. 6

Activation of WNT-signalling may contribute to survival of UCCs upon long-term cisplatin treatment. a Morphology of RT-112-LTT and J82-LTT and their parental cell lines. Scale bars, 100 μm. qRT-PCR demonstrated relative expression levels of E-Cadherin, Vimentin, Twist1, ZEB1 (b) and CLDN3 and CLDN4 (c) in RT-112-LTT and J82-LTT and their parental cell lines. d Immunofluorescence stainings for E-cadherin and Vimentin (d) and β-Catenin (e) in RT-112-LTT and J82-LTT and their parental cell lines. DAPI staining (blue) was used to visualize nuclei. Scale bars, 50 μm. f Relative RNA expression levels of β-Catenin, AXIN-2, CCDN1, c-MYC, and PITX2 in untreated and RT-112-LTT and J82-LTT. Expression levels in the untreated control were set as 1. g Basal and inducible activity of a TCF/β-Catenin-dependent promotor. Mean ± SD of duplicates of TopFlash/FopFlash and TopFlash+S33Y/TopFlash ratio are shown in RT-112-LTT and J82-LTT and their parental cell lines. 22RV1 and HepG2 cell lines were used as controls. h Relative cell viability was measured 72 h after treatment with cisplatin, niclosamide, or combination of both by MTT assay in RT-112-LTT and J82-LTT. *P <0.05; **P <0.001

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