Cancer Cell International (Sep 2018)

MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3

  • Yong-Xia Wang,
  • Hui-Fang Zhu,
  • Zhe-Ying Zhang,
  • Feng Ren,
  • Yu-Han Hu

DOI
https://doi.org/10.1186/s12935-018-0628-6
Journal volume & issue
Vol. 18, no. 1
pp. 1 – 10

Abstract

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Abstract Background Growing evidence suggests that MiRNAs play essential roles in the initiation and progression of colorectal cancer (CRC). The aberrant expression of miR-384 has been reported in some cancers. However, the role and mechanism of miR-384 in CRC proliferation remains unknown. Methods The expression of miR-384 was detected in CRC and their paired normal tissues by real-time PCR. In vivo and in vitro assays were conducted to confirm the role of miR-384 in the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro assays were used to confirm that AKT3 was the target gene of miR-384. Finally, Spearman’s correlation analyses was carried out to analyze the relationship between miR-384 expression and AKT3 expression in CRC. Results MiR-384 was down‑regulated in CRC tissues. The in vivo and vitro functional assays verified that the ectopic upregulation of miR-384 inhibited the proliferation of CRC and the inhibition of miR-384 promoted the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro functional assays confirmed AKT3 as the target gene of miR-384. The expression of miR-384 was negatively correlated with the expressions of AKT3. Conclusion Our study verified that miR-384 could significantly suppress the proliferation of CRC by directing targeting AKT3.

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