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Fig. 1 | Journal of Translational Medicine

Fig. 1

From: Targeting RPA promotes autophagic flux and the antitumor response to radiation in nasopharyngeal carcinoma

Fig. 1

The RPAi HAMNO impairs the aggressive phenotype of NPC cells. a Cell growth curves for DMSO- and HAMNO-treated (10/20 μM) 5-8F, S26 and CNE2 cells at the indicated times. b Inhibition of RPA by HAMNO treatment impairs in vitro colony formation in DMSO- and HAMNO-treated (10/20 μM) NPC cell lines. Crystal violet staining of representative cells from three separate studies is shown (left). Focal adhesions were counted (on the right). c Representative images of tumorspheres and quantification of diameters from 5-8F and S26 cells. Soft agar colony formation assay of 5-8F and S26 cell lines treated with HAMNO (0, 10, 20 μM) for 12 days after seeding. Magnification, × 10. d–g The image shows the sizes of the tumors in nude mouse xenograft models at the end of the experiment D. Scale bar, 1 cm. Xenograft tumor growth curve E, weight F and mouse body weight G of S26 cells in nude mice treated with HAMNO at 2 mg/kg. Error bars in e and g mean ± SEM (n = 6 per group). ns = nonsignificant, two-way ANOVA with Dunnett’s multiple comparisons test. Data in f are shown as the mean ± SD (n = 6/group). Student’s t test. h Tumor slices from mice that were treated differently were stained with hematoxylin and eosin (HE) and IHC for Ki-67 and cleaved caspase 3 (left). Scale bar = 100 μm or 25 μm. The percentage of tumor cells that were positive for Ki-67 and cleaved caspase-3 in the various S26 xenograft tumor groups (right). The statistical analysis for H was performed using the Kolmogorov‒Smirnov test, and the data are presented as medians with 95% CI

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