NF-κB1, c-Rel, and ELK1 inhibit miR-134 expression leading to TAB1 upregulation in paclitaxel-resistant human ovarian cancer

Oncotarget. 2017 Apr 11;8(15):24853-24868. doi: 10.18632/oncotarget.15267.

Abstract

The mechanism by which the transcription factors inhibit the miRNA expression in ovarian cancer chemoresistance is unclear. The present study investigated the mechanism underlying the transcriptional repression of miR-134 in chemoresistant serous epithelial ovarian cancer. The results demonstrate that NF-κB1, c-Rel, and ELK1 are involved as transcription factors in repressing miR-134 expression in paclitaxel-resistant ovarian cancer cells. Knockdown of these transcription factors led to increased miR-134 expression, resulting in increased apoptosis and inhibition of proliferation in SKOV3-TR30 cells. NF-κB1, c-Rel, and ELK1 mRNA expression was upregulated in chemoresistant specimens and negatively correlated with miR-134 expression. Kaplan-Meier analysis revealed that high nuclear expressions of NF-κB1, c-Rel, ELK1 were significantly associated with short survival in serous epithelial ovarian cancer patients. Finally, TAB1 was identified as a functional target of miR-134, and the expression of TAB1 was increased by the transcription factors of NF-κB1, c-Rel, and ELK1 via miR-134. Taken together, these results provide an insight into the mechanism of repressed miR-134 expression in chemoresistance of serous epithelial ovarian cancer.

Keywords: miR-134; miRNA gene regulation; ovarian cancer; paclitaxel resistance; transcription factor.

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / metabolism*
  • Drug Resistance, Neoplasm
  • Female
  • Gene Knockdown Techniques
  • Humans
  • MicroRNAs / antagonists & inhibitors*
  • MicroRNAs / biosynthesis
  • MicroRNAs / genetics
  • MicroRNAs / metabolism
  • NF-kappa B / genetics
  • NF-kappa B / metabolism*
  • Ovarian Neoplasms / drug therapy
  • Ovarian Neoplasms / genetics
  • Ovarian Neoplasms / metabolism*
  • Paclitaxel / pharmacology*
  • Proto-Oncogene Proteins c-rel / metabolism*
  • Transcription Factors / metabolism
  • Transfection
  • Up-Regulation
  • ets-Domain Protein Elk-1 / genetics
  • ets-Domain Protein Elk-1 / metabolism*

Substances

  • Adaptor Proteins, Signal Transducing
  • ELK1 protein, human
  • MIRN134 microRNA, human
  • MicroRNAs
  • NF-kappa B
  • Proto-Oncogene Proteins c-rel
  • REL protein, human
  • TAB1 protein, human
  • Transcription Factors
  • ets-Domain Protein Elk-1
  • Paclitaxel