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. 2022 Mar 28;22(1):145.
doi: 10.1186/s12876-022-02203-2.

MiR-1-3p targets CENPF to repress tumor-relevant functions of gastric cancer cells

Affiliations

MiR-1-3p targets CENPF to repress tumor-relevant functions of gastric cancer cells

Shenkang Zhou et al. BMC Gastroenterol. .

Abstract

Here we noted significantly downregulated miR-1-3p in gastric cancer (GC) tissue compared with adjacent normal tissue through qRT-PCR. Lowly expressed miR-1-3p correlated GC progression. Overexpressing miR-1-3p could restrain tumor-relevant cell behaviors in GC, while miR-1-3p inhibitor treatment triggered the opposite results. Moreover, dual-luciferase reporter gene detection identified specific binding sites of miR-1-3p in CENPF 3'untranslated region. Upregulating miR-1-3p constrained cell progression of GC via CENPF downregulation. Western blot, qRT-PCR and dual-luciferase detections manifested that miR-1-3p negatively mediated CENPF expression in GC cells. Thus, we demonstrated that miR-1-3p negatively mediated CENPF to hamper GC progression. CENPF may be an underlying target for GC therapy.

Keywords: CENPF; Gastric cancer; Invasion and migration; Proliferation; miR-1-3p.

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Conflict of interest statement

All authors confirm no conflicts of interest in this work.

Figures

Fig. 1
Fig. 1
MiR-1-3p is downregulated in GC tissue and cells. A Compared with normal tissue, miR-1-3p was markedly down-regulated in tumor tissue according to data from TCGA and analyzed by two-tailed test; B MiR-1-3p level at cellular level. *p < 0.05
Fig. 2
Fig. 2
MiR-1-3p overexpression hampers GC cell proliferation, invasion and migration. A Level of miR-1-3p upon transfection; BE Cell functions after transfection were measured by CCK-8, colony formation, wounding healing (40 ×) and Transwell (100 ×) methods. *p < 0.05
Fig. 3
Fig. 3
CENPF is a direct target of miR-1-3p. A Volcano plot of DEmRNAs in TCGA-STAD. Red: differentially upregulated genes; green: differentially downregulated genes; B Venn diagram of predict upregulate genes and target genes; C Pearson correlation analysis between miR-1-3p and 6 target mRNAs; D Upregulated CENPF as tested by two-tail test; E, F mRNA and protein levels of CENPF in each group; G Putative binding sites of CENPF 3’UTR and miR-1-3p. Mutations were generated in the 3′-UTR of CENPF by mutated seed matching sequences; H Dual-luciferase detected luciferase activity in co-transfected cells. *p < 0.05
Fig. 4
Fig. 4
MiR-1-3p modulates GC cell functions through targeting CENPF. A, B qRT-PCR and western blot were used to measure the mRNA and protein expression levels of CENPF in MGC803 and AGS cells in each group; CF GC cell functions after transfection were measured by CCK-8, colony formation, wounding healing (40 ×) and Transwell (100 ×) methods. *p < 0.05

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