Open Access

miR‑27a‑3p regulates proliferation and apoptosis of colon cancer cells by potentially targeting BTG1

  • Authors:
    • Chang Su
    • Dong‑Ping Huang
    • Jian‑Wen Liu
    • Wei‑Yan Liu
    • Yi‑Ou Cao
  • View Affiliations

  • Published online on: July 18, 2019     https://doi.org/10.3892/ol.2019.10629
  • Pages: 2825-2834
  • Copyright: © Su et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

microRNA (miR/miRNA)‑27a‑3p has been reported to be abnormally expressed in various types of cancer, including colorectal cancer (CRC). B‑cell translocation gene 1 (BTG1) has also been implicated with CRC. However, the association between miR‑27a‑3p and BTG1 in CRC, to the best of our knowledge, has not been investigated. In order to assess whether miR‑27a‑3p is associated with CRC, reverse transcription‑quantitative PCR was performed on 20 paired CRC and paracancerous tissues for miRNA analysis. For the screening and validation of miR‑27a‑3p expression in colon cancer, several colon cancer cell lines (HCT‑116, HCT8, SW480, HT29, LOVO and Caco2) and the normal colorectal epithelial cell line NCM460 were examined. The highest expression levels of miR‑27a‑3p were detected in the HCT‑116, which was selected for further experimentation. The HCT‑116 cells were divided into control, miR‑27a‑3p mimic and inhibitor groups, and cell proliferation was tested using an MTT assay. Additionally, miR‑27a‑3p inhibitor/mimic or BTG1 plasmid were transfected into the HCT‑116 cells, and flow cytometry was performed to analyze cell cycle distributions. TUNEL analysis was performed to detect apoptosis. Protein levels of factors in the downstream signaling pathway mediated by miR‑27a‑3p [ERK/mitogen‑activated extracellular signal‑regulated kinase (MEK)] were detected. miR‑27a‑3p was revealed to be overexpressed in human CRC tissues and colon cancer cell lines. Knockdown of miR‑27a‑3p suppressed proliferation of HCT‑116 cells and apoptosis was increased. It further markedly upregulated expression levels of BTG1 and inhibited activation of proteins of the ERK/MEK signaling pathway. In addition, overexpression of BTG1 in HCT‑116 cells triggered G1/S phase cell cycle arrest and increased apoptosis via the ERK/MEK signaling pathway. In conclusion, the present study demonstrated that the effects of miR‑27a‑3p on colon cancer cell proliferation and apoptosis were similar to those of the tumor suppressor gene BTG1. The miR‑27a‑3p/BTG1 axis may have potential implications for diagnostic and therapeutic approaches in CRC.
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September 2019
Volume 18 Issue 3

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Copy and paste a formatted citation
APA
Su, C., Huang, D., Liu, J., Liu, W., & Cao, Y. (2019). miR‑27a‑3p regulates proliferation and apoptosis of colon cancer cells by potentially targeting BTG1. Oncology Letters, 18, 2825-2834. https://doi.org/10.3892/ol.2019.10629
MLA
Su, C., Huang, D., Liu, J., Liu, W., Cao, Y."miR‑27a‑3p regulates proliferation and apoptosis of colon cancer cells by potentially targeting BTG1". Oncology Letters 18.3 (2019): 2825-2834.
Chicago
Su, C., Huang, D., Liu, J., Liu, W., Cao, Y."miR‑27a‑3p regulates proliferation and apoptosis of colon cancer cells by potentially targeting BTG1". Oncology Letters 18, no. 3 (2019): 2825-2834. https://doi.org/10.3892/ol.2019.10629