HOXD3 targeted by miR-203a suppresses cell metastasis and angiogenesis through VEGFR in human hepatocellular carcinoma cells

Sci Rep. 2018 Feb 5;8(1):2431. doi: 10.1038/s41598-018-20859-3.

Abstract

Hepatocellular carcinoma (HCC), one of the most common aggressive tumors worldwide has a relatively high mortality rate among malignant tumors. MicroRNAs (miRNAs), acting as tumor suppressors, are involved in the regulation of invasion, metastasis, and angiogenesis of tumor cells. However, a potential role for miR-203a in HCC has not been described yet. In this study, we show that miR-203a markedly suppresses HCC cell migration, invasion, and angiogenesis. In addition, the transcription factor HOXD3 appears to be a direct target of miR-203a. HOXD3 knockdown substantially decreased HCC cell migration, invasion, and angiogenesis, effects similar to those seen for miR-203a expression. Rescuing the function of HOXD3 attenuated the effect of miR-203a overexpression in HCC cells. Furthermore, HOXD3 can directly target the promoter region of VEGFR and increase VEGFR expression. Taken together, our findings indicate that miR-203a inhibits HCC cell invasion, metastasis, and angiogenesis by negatively targeting HOXD3 and suppressing cell signaling through the VEGFR pathway, suggesting that miR-203a might represent a potential therapeutic target for HCC intervention.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Hepatocellular / genetics*
  • Carcinoma, Hepatocellular / metabolism
  • Carcinoma, Hepatocellular / pathology
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • Diffusion Chambers, Culture
  • Gene Expression Regulation, Neoplastic*
  • Hepatocytes / metabolism
  • Hepatocytes / pathology
  • Homeodomain Proteins / antagonists & inhibitors
  • Homeodomain Proteins / genetics*
  • Homeodomain Proteins / metabolism
  • Humans
  • Liver Neoplasms / genetics*
  • Liver Neoplasms / metabolism
  • Liver Neoplasms / pathology
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Neovascularization, Pathologic / genetics*
  • Neovascularization, Pathologic / metabolism
  • Neovascularization, Pathologic / pathology
  • Plasmids / chemistry
  • Plasmids / metabolism
  • Promoter Regions, Genetic
  • Protein Binding
  • RNA, Small Interfering / genetics
  • RNA, Small Interfering / metabolism
  • Signal Transduction
  • Transcription Factors
  • Vascular Endothelial Growth Factor Receptor-1 / genetics*
  • Vascular Endothelial Growth Factor Receptor-1 / metabolism

Substances

  • Homeodomain Proteins
  • MIRN203 microRNA, human
  • MicroRNAs
  • RNA, Small Interfering
  • Transcription Factors
  • HOXA4 protein, human
  • Vascular Endothelial Growth Factor Receptor-1