Fig. 7.

LINC01234 upregulates SHMT2 expression by competitively binding to miR-642a-5p. a qRT-PCR analysis of miR-642a-5p expression in LoVo cells and HCT116 cells transfected with negative control (NC), sh-LINC01234 or LINC01234-expressing vectors. b Schematic view of the miR-642a-5p putative targeting site in the WT and MUT of LINC01234. c The luciferase reporter plasmid containing wild-type (WT) or mutant (MUT) LINC01234 was cotransfected into LoVo cells and HCT116 cells with miR-642a-5p. d The RNA levels in RNA immunoprecipitates are presented as the fold enrichment in Ago2 relative to IgG immunoprecipitates. e Schematic view of the miR-642a-5p putative targeting site in the WT and MUT 3’-UTR of SHMT2. f The luciferase reporter plasmid containing wild-type (WT) or mutant (MUT) 3’-UTR of SHMT2 was cotransfected into LoVo cells and HCT116 cells with miR-642a-5p. g qRT-PCR analysis of SHMT2 expression in LoVo cells and HCT116 cells transfected with control, miR-642a-5p inhibitor, negative control (NC) or miR-642a-5p mimic. h Western blot analysis of SHMT2 expression in LoVo cells and HCT116 cells transfected with control, miR-642a-5p inhibitor, negative control (NC) or miR-642a-5p mimic. i qRT-PCR analysis of SHMT2 expression in LoVo cells and HCT116 cells transfected with sh-NC, sh-LINC01234, or cotransfected sh-LINC01234 and miR-642a-5p inhibitor. j Western blot analysis of SHMT2 expression in LoVo cells and HCT116 cells transfected with sh-NC, sh-LINC01234, or cotransfected sh-LINC01234 and miR-642a-5p inhibitor. The experiments were performed in triplicate. The data are represented as means ± SD from three independent experiments. *P < 0.05