Fig. 5

DCA enhances the NDV-mediated oncolysis and antitumour efficacy in HCC. a, b Cells were infected with NDV (MOI = 10) in the presence or absence of DCA (20 mM) for 48 h, and the oncolytic effects were determined by MTT assays (a) and trypan-blue exclusion assays (b). Means and standard deviations of quadruplicate samples are shown. c Cells were seeded in 96-well plates and infected with NDV at various MOIs (0, 1, 2, 5, 10, 20, 40, and 80) for 48 h, with or without DCA (20 mM). Cell viability was assessed by MTT assays. Means and standard deviations of quadruplicate samples and IC₅₀ (half maximal inhibitory concentration) values of NDV are shown. d, e Mice were treated as previously described (Fig. 1I), ascitic cells were harvested after 10 or 15 days and cell numbers were determined by trypan-blue exclusion assays (d); means and standard deviations of five mice are shown. Kaplan–Meier survival curves were plotted (e) and analysed by log-rank (Mantel–Cox) test. All mice in each group were included in each analysis. f–h Mice were injected subcutaneously with 5 × 10⁶ Hepa1-6 cells. On days 7, 10, and 13, the mice received an intratumoural injection of 1 × 10⁷ pfu NDV, with or without DCA (200 mg/kg, daily, i.g.) (f). Tumour volumes were measured by calliper every 2–3 days before treatment; means and standard deviations of each group are shown (g). Kaplan–Meier survival curves were plotted (h) and analysed by log-rank (Mantel–Cox) test. All mice in each group were included in each analysis. *, p < 0.05; ***, p < 0.001