Fig. 2

MiR-105-5p is sponged by MCF2L-AS1 and acts as a tumor-suppressor gene in CRC. A and B. The location of MCF2L-AS1 in CRC cells was assessed by subcellular fractionation and FISH assays. C. The enrichment of MCF2L-AS1 in RISC was tested via RIP assay. D. The potential miRNAs that could bind to MCF2L-AS1 was displayed (left). RT-qPCR assay was used to test the expression of seven potential miRNAs that could bind to MCF2L-AS1 (right). E. The binding capacity between MCF2L-AS1 and miR-105-5p was verified through RNA pull down assay. F. The binding sites between MCF2L-AS1 and miR-105-5p were predicted by ENCORI website. G. The overexpression efficiency of miR-105-5p was examined by RT-qPCR assay. H. Luciferase reporter assay was carried out to testify the combination between MCF2L-AS1 and miR-105-5p. I and J. Cell proliferation effected by miR-105-5p overexpression was detected by IF and EdU assays. K and L. Cell migration and invasion upon miR-105-5p overexpression were evaluated by Transwell assay. M and N. Cell apoptosis was assessed by flow cytometry assay and caspase-3/8/9 activity analysis. O. The EMT process upon miR-105-5p overexpression was measured through IF assay. Adjustments of individual color channels were made on ‘Merge’ figures. The statistical analysis of Fig. 2H was tested with two-way ANOVA, and the statistical analysis of Fig. 2B-E, G, I-N was tested with one-way ANOVA. **P < 0.01