Fig. 6

CircNTRK2 promotes ESCC cell malignant behaviors by modulating NRIP1 expression. (a) The protein level of NRIP1 in si-NRIP1-transfected Eca-109 and KYSE-150 cells was determined by western blot assay. (b) The effect of NRIP1 knockdown on cell viability was assessed by CCK-8 assay. (c) Colony formation assay in Eca-109 and KYSE-150 cells with NRIP1 depletion. (d) Transwell assay was used to evaluate the effect of NRIP1 down-regulation on cell invasive capacity. (e) Flow cytometry was performed to measure the apoptotic rate of Eca-109 and KYSE-150 cells transfected with si-NRIP1. (f) The protein levels of cleaved PARP, cleaved caspase-3, E-cadherin and vimentin were examined by western blot assay in Eca-109 and KYSE-150 cells. (g-j) Eca-109 cells were transfected with si-NC, si-circ #2 or si-circ #2 + NRIP1, followed by (g) western blot assay to evaluate the protein level of NRIP1; (h) CCK-8 assay to determine cell viability; (i) colony forming assay to detect colony-formation ability; (j) transwell assay to examine cell invasiveness. (k) The schematic diagram shows that circNTRK2 acts as a sponge for miR-140-3p to relieve its suppression on NRIP1 expression, thereby contributing to ESCC proliferation and metastasis. *P < 0.05, **P < 0.01