Fig. 8

Expression of circNRIP1 in GC can be regulated by QKI. a. We constructed a series of mutation plasmids (pZW1) consisting of either mutated I1QB or I3QB (#1, #2) or both I1QB and I3QB (#3), and we also constructed a wild-type plasmid spanning intron 1 to intron 3 (#4). b. We observed that only the wild-type plasmid (#4), and neither the I1QB nor I3QB deletion constructs (#1–3), could overexpress circNRIP1 according to northern blotting of GC cells.c. We observed that only the wild-type plasmid (#4), and neither the I1QB nor I3QB deletion constructs (#1–3), could overexpress circNRIP1 according to qRT-PCR in GC cells. d. We knocked down QKI and observed a significant reduction in circNRIP1 but not pre-mNRIP1 or mNRIP1. e. Enrichment of I1QB and I3QB was observed when we used an antibody against QKI. f. We detected higher QKI expression level in GC tumour tissues relative to adjacent normal stomach tissues among 40 patients by immunohistochemistry, scale bar = 200 μm. g. We performed qRT-PCR on these 40 patients and discovered that the expression level of circNRIP1 was positively related to the QKI histochemistry score. All data are presented as the mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001