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The long non‑coding RNA (lncRNA) differentiation antagonizing non‑protein coding RNA (DANCR) has been reported to be a novel potential biomarker for colon cancer prognosis. However, its functional role in colon cancer remains unknown. In the present study, DANCR expression in colon cancer cell lines was determined by reverse transcription‑quantitative polymerase chain reaction. Cell Counting kit‑8 assay, colony formation assay, flow cytometry, Hoechst 33258 staining and western blotting were utilized to investigate the effect and mechanism of DANCR in the regulation of colon cancer growth. Establishment of a xenograft tumor model followed by terminal deoxynucleotidyl transferase (TdT) dUTP nick‑end labeling assay and immunohistochemical staining were performed to confirm the findings in vitro. DANCR was revealed to be overexpressed in all human colon cancer cell lines. Silencing DANCR by small interfering RNA significantly inhibited cell proliferation and colony formation. Flow cytometry analyses and Hoechst 33258 staining revealed that apoptosis was induced upon DANCR‑knockdown. Silencing DANCR was revealed to efficiently impair colon tumor growth by promoting caspase 3 expression and tumor apoptosis. In summary, the results of the present study demonstrated that DANCR is a potential therapeutic target in colon cancer. [ABSTRACT FROM AUTHOR]

The aim of the current study was to investigate the expression and role of microRNA-486-5p (miR-486-5p) in hypertrophic scar (HS) formation, and to examine the associated mechanisms. First, miR-486-5p expression was detected in HS tissues and human hypertrophic scar fibroblasts (hHSFs) by reverse transcription-quantitative polymerase chain reaction. Target genes of miR-486-5p were predicted using TargetScan and verified by dual-luciferase reporter assays. To investigate the role of miR-486-5p in HS formation, miR-486-5p was overexpressed in hHSFs through transfection with miR-486-5p mimics. MTT, cell apoptosis and cell cycle assays were preformed to investigate the proliferation, cell apoptosis and cell cycle distribution of hHSFs, respectively. Additionally, protein expression was measured by western blot analysis. The results demonstrated that miR-486-5p expression was significantly decreased in HS tissues and cells. Mothers against decapentaplegic homolog (Smad)2 was a target gene of miR-486-5p, and it was negatively regulated by miR-486-5p. It was also found that Smad2 expression was significantly increased in HS tissues and cells. Further analysis indicated that miR-486-5p mimic transfection inhibited the proliferation, induced cell apoptosis and increased G1/S phase arrest in hHSFs. Furthermore, the expression of cyclin-dependent kinase (CDK)2, CDK4 and apoptosis regulator Bcl-2 was repressed, while apoptosis regulator BAX expression was enhanced by miR-486-5p mimic transfection. Notably, the effects of miR-486-5p mimic on hHSFs were significantly eliminated by Smad2 plasmid transfection. Taken together, these results demonstrated that miR-486-5p inhibited the proliferation, induced apoptosis and increased G1/S phase arrest of hHSFs by targeting Smad2. miR-486-5p may be a promising therapeutic target for HS management. [ABSTRACT FROM AUTHOR]