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. 2020 Oct 19;21(11):1025–1032. doi: 10.1080/15384047.2020.1824514

Figure 2.

Figure 2.

MiR-2116-3p could directly bind to FALEC

A–B. The subcellular localization of FALEC in LoVo and HCT8 cells was detected by subcellular fractionation and FISH assays. C. qRT-PCR analysis was performed to evaluate the expression of candidate miRNAs in LoVo cells after knockdown of FALEC. D. The expression of miR-2116-3p in CRC cell lines and normal NCM460 cells was detected by qRT-PCR. E. Putative binding sequences between miR-2116-3p and FALEC predicted by DIANA, as well as the sequence of FALEC-MUT with such binding sites mutated. F. Dual luciferase reporter assays demonstrated that miR-2116-3p overexpression successfully decreased the luciferase activity of FALEC-WT. G. RNA pull down assay showed that miR-2116-3p was preferentially enriched by biotin-labeled FALEC-WT. H. The expression of miR-2116-3p was evaluated via qRT-PCR in CRC cells with the transfection of miR-2116-3p inhibitor. I–N. Rescue experiments were performed in LoVo and HCT8 cells to explore the effects of miR-2116-3p inhibitor on sh-FALEC#1-transfected cell proliferation, apoptosis, migration, invasion and angiogenesis. **P < .01.