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Fig. 3 | Molecular Cancer

Fig. 3

From: Up-regulated NRIP2 in colorectal cancer initiating cells modulates the Wnt pathway by targeting RORβ

Fig. 3

NRIP2 up-regulates Wnt pathway activity. a Over-expression of NRIP2 up-regulates Wnt pathway activity. c-Myc and cyclin D1 were detected by western blotting in HT29, P1, and SW620 cells infected with recombinant lentivirus encoding NRIP2 with Myc-Tag, with cells infected with blank lentivirus as controls. b Wnt activity in NRIP2-knockdown cells. c-Myc and cyclin D1 were detected by western blotting in NRIP2-knockdown HT29, P1, and SW620 cells and their scrambled shRNA-treated cells (controls). c Quantification of colospheres after NRIP2 silence. The number of colospheres was counted in Nrip2-expressing HT29 and P1 cells after NRIP2 silence. The number of colospheres significantly decreased after silence of NRIP2, *p < 0.05 (ANOVA). Transfection with RNAi scramble as controls. d Quantification of colospheres in NRIP2-overexpressing cells after Wnt inactivation. Colospheres were counted in NRIP2-overexpressing HT29, P1, and SW620 cells and controls treated with Wnt (7.2 μM) and β-catenin inhibitors (3.6 μM). The colosphere number significantly decreased in NRIP2-overexpressing cells after Wnt inactivation. *p < 0.05; **p < 0.01 (ANOVA). e Tumorigenicity of NRIP2- overexpressing cells. NRIP2- overexpressing P1 and HT29 cells and their control cells infected with blank lentivirus were injected into naked Balb/c mice, respectively. Tumor formation was quantified within 4 weeks. The results showed that overexpression of NRIP2 significantly increased tumorigenicity (# p < 0.05, Multivariate logistic analysis)

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