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Previous studies have demonstrated that microRNAs (miRs) are involved in the carcinogenesis of colorectal cancer (CRC). To the best of our knowledge, the function and regulatory role of miR-532-5p in human CRC remains unknown. The aim of the present study was to determine the role and regulation of miR-532-5p in CRC. Using the reverse transcription-quantitative polymerase chain reaction, it was demonstrated that miR-532-5p was upregulated, whereas runt-related transcription factor 3 (RUNX3) was downregulated in CRC tissues. The upregulated miR-532-5p was associated with the downregulated RUNX3. Furthermore, the two biomarkers were associated with numerous clinicopathological characteristics of CRC, including tumor stage, lymph node involvement, differentiation, vessel invasion and tumor recurrence. The in vitro luciferase reporter assay demonstrated that transfection with miR-532-5p mimic markedly downregulated the RUNX3 mRNA and protein levels, via specific binding to the 5'-untranslated region of RUNX3 in human HT-29 CRC cells. In addition, an MTT assay and a colony formation assay demonstrated that miR-532-5p overexpression led to increased tumor cell viability and colony formation ability of HT-29 cells. In conclusion, the results of the present study indicate that miR-532-5p may function as an oncogenic miRNA by promoting cell growth in human CRC cells, and such promotion is associated with the targeted inhibition of RUNX3.

Oncogenic role of microRNA-532‑5p in human colorectal cancer via targeting of the 5'UTR of RUNX3