Fig. 5
From: The long non-coding RNA CYTOR drives colorectal cancer progression by interacting with NCL and Sam68
Production of CYTOR mutant cells by CRISPR/Cas9. a Prediction of secondary RNA structure of wild-type (WT) CYTOR and various exon-deleted CYTOR mutants. b Schematic diagram for CRISPR/Cas9 and donor vector to delete EXON1 or EXON4 of CYTOR. c RT-PCR and gel electrophoresis to assess the editing efficiency of CRISPR-sgRNA specific to EXON 1. *indicates Non-homologous end joining with an Indel. d RT-PCR and gel electrophoresis to assess the editing efficiency of CRISPR-sgRNA specific to EXON 4. *indicates Non-homologous end joining with an Indel. e DNA sequencing to identify the exon1-deleted RKO cells (ΔEXON1) through clone screening. f DNA sequencing to identify the exon4-deleted RKO cells (ΔEXON4) through clone screening