Fig. 6.

PrxII inhibition blocks the tumorigenic growth of APC-mutant CRC cells xenografted to mice. a Expression levels of PrxI and PrxII genes in healthy individuals (Normal, n = 26) and patients with colorectal cancer. (CRC, n = 155) from the TCGA COAD database. Box plot represents the average expression of PrxI and PrxII ± s.d. The horizontal line indicates the median value. b PrxII immunostaining in the colon tissue array from healthy individuals (Normal, n = 5) and patients with colon cancer (CRC, n = 45). The IHC images were quantified using the HistoFAXS Tissue Analysis System. Data in the graph are mean intensities ± s.d. The average intensities and P value are indicated. Scale bar, 50 μm. c Purified recombinant PrxI and PrxII enzymes were pre-incubated with conoidin A (10 μM) in the reaction mixture for 5 min before H₂O₂ addition. The NADPH reduction was monitored by light absorption at 340 nm. Reaction curves shown are means ± s.d. of three independent experiments. d HT29, SW480, and RKO cells were grown in the presence of control vehicle or conoidin A for 10 days, and the colonies were stained with crystal violet and counted. Data in the graph are the average number of colonies ± s.d. (n = 3, *P < 0.02, **P < 0.01, ^# P < 0.0001). NS, statistically not significant. e HT29-luc2 cells were injected to athymic nu/nu mice and grown for 6 days before first i.p. administration of conoidin A (Arrowhead). Conoidin A was administered every 3 days for 28 days (1 mg conoidin A per kg body weight per injection). The bioluminescent signals were taken as described in the Methods. Data in the graph are the mean photon numbers per second ± s.d. (n = 7 mice per group, *P < 0.0001 with repeated-measured ANOVA). A representative image is shown. f After 28 days, the HT29 Luc2-driven tumor tissues were removed, weighed and photographed. Graph shows the average mass ± s.d. of the isolated tumors (n = 7 mice per group, *P < 0.005). Scale bar, 10 mm