MiRNA-224-5p inhibits autophagy in breast cancer cells via targeting Smad4

Biochem Biophys Res Commun. 2018 Dec 2;506(4):793-798. doi: 10.1016/j.bbrc.2018.10.150. Epub 2018 Oct 30.

Abstract

Autophagy is known as a protective intracellular procedure, which can be regulated by several factors. MiRNA has been suggested as a potential element to mediate autophagy pathway in carcinomas. Our study was aim to investigate the role of autophagy in breast cancer cells and identify the involved molecular mechanism METHODS: The expression of LC3I/II, SQSTM1 and Smad4 were detected by western blot. The mRNA level were quantified by real-time PCR. MDC staining was used to directly visualize autophagosome formation. Target Scan 7.2 was used to predict biological targets of miR-224-5p RESULTS: MiR-224 -5p expression was upregulated in metastatic breast cancer and non-metastatic breast cancer cells compare with control. Moreover, miR-224-5p inhibition enhanced cellular autophagy levels in breast cancer cells. MiR-224-5p could suppress Smad4 expression in MDA-MB-231 cells, which indicated that Smad4 was identified as a target of miR-224-5p in breast cancer cells with high metastatic potential CONCLUSIONS: Our study revealed that miR-224-5p inhibited autophagy by targeting Smad4 in MDA-MB-231 cells. The results indicated that miR-224-5p/Smad4 regulating autophagy might be a novel regulatory network contributing to metastasis of breast cancer. MiR-224-5p and Smad4 is involved in breast tumorigenesis, which is possibly a novel target for breast cancer therapy.

Keywords: Autophagy; Breast cancer; Metastasis; Smad4; miR-224-5p.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Autophagy*
  • Base Sequence
  • Breast Neoplasms / blood
  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology*
  • Case-Control Studies
  • Cell Line, Tumor
  • Female
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic
  • Humans
  • MicroRNAs / metabolism*
  • Neoplasm Metastasis
  • Smad4 Protein / metabolism*

Substances

  • MIRN224 microRNA, human
  • MicroRNAs
  • SMAD4 protein, human
  • Smad4 Protein