cir-ITCH plays an inhibitory role in colorectal cancer by regulating the Wnt/β-catenin pathway

PLoS One. 2015 Jun 25;10(6):e0131225. doi: 10.1371/journal.pone.0131225. eCollection 2015.

Abstract

Noncoding RNAs (ncRNAs) are the dominant product of eukaryotic transcription. These products range from short microRNAs (miRNAs) to long intergenic noncoding RNAs (lincRNAs). Circular RNAs composed of exonic sequences represent an understudied form of ncRNA that was discovered more than 20 years ago. Using a TaqMan-based reverse transcriptase polymerase chain reaction assay, we analyzed the relationship between cir-ITCH expression and colorectal cancer (CRC) in a total of 45 CRCs and paired adjacent non-tumor tissue samples. We found that cir-ITCH expression was typically down-regulated in CRC compared to the peritumoral tissue. This result, as well as several follow-up experiments, showed that cir-ITCH could increase the level of ITCH, which is involved in the inhibition of the Wnt/β-catenin pathway. Therefore, our results showed that cir-ITCH plays a role in CRC by regulating the Wnt/β-catenin pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3' Untranslated Regions
  • Adult
  • Binding Sites
  • Cell Survival
  • Colorectal Neoplasms / metabolism*
  • Dactinomycin / chemistry
  • Exoribonucleases / chemistry
  • Female
  • Gene Expression Regulation, Neoplastic*
  • HCT116 Cells
  • Humans
  • Male
  • MicroRNAs / metabolism*
  • Middle Aged
  • Plasmids / metabolism
  • RNA / metabolism*
  • RNA, Circular
  • RNA, Untranslated / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Wnt Proteins / metabolism
  • Wnt Signaling Pathway*
  • beta Catenin / metabolism

Substances

  • 3' Untranslated Regions
  • MicroRNAs
  • RNA, Circular
  • RNA, Untranslated
  • Wnt Proteins
  • beta Catenin
  • cir-ITCH noncoding RNA, human
  • Dactinomycin
  • RNA
  • Exoribonucleases
  • ribonuclease R

Grants and funding

This work was supported by a grant from Wenzhou Science and Technology Bureau Natural Science Foundation (Y20140700 Dr. XC). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.