The mechanism of all-trans retinoic acid-induced cleft palate may be related to the novel ENSMUST00000159153-miR-137-5p-Wnt7a and ENSMUST000000236086-miR-34b-3p-EphA10/TRPM2 ceRNA crosstalk

Environ Toxicol Pharmacol. 2025 Mar:114:104623. doi: 10.1016/j.etap.2024.104623. Epub 2024 Dec 20.

Abstract

Cleft palate is the most prevalent congenital condition. Cleft palate is brought on by an exogenous chemical called all-trans retinoic acid (atRA). In order to indirectly control gene expression, long chain non-coding RNAs (lncRNAs) act as competitive endogenous RNA (ceRNA) sponges. Its exact mode of action in cleft palate has not yet been determined. The purpose of this study was to determine whether lncRNAs and miRNAs regulated palatal fusion genes during the formation of cleft palate and to offer a possible course for cleft palate target gene therapy. In this work, we created a cleft palate model using atRA, conducted RNA sequencing (RNA-seq) to identify the genes that differed between the atRA-treated group and the control group, and built the lncRNA-miRNA-mRNA ceRNA network based on the projected ceRNA. The results were confirmed using a quantitative real-time polymerase chain reaction (qRT-PCR). ENSMUST00000159153-miR-137-5p-Wnt7a and ENSMUST000000236086-miR-34b-3p-EphA10/TRPM2 may be the main causes of atRA-induced cleft palate, according to the results.

Keywords: All trans retinoic acid; Cleft palate; Competing endogenous RNA; Long non-coding RNA; MicroRNA.

MeSH terms

  • Animals
  • Cleft Palate* / chemically induced
  • Cleft Palate* / genetics
  • Male
  • Mice
  • MicroRNAs / genetics
  • RNA, Competitive Endogenous
  • RNA, Long Noncoding* / genetics
  • TRPM Cation Channels / genetics
  • Tretinoin* / toxicity
  • Wnt Proteins / genetics

Substances

  • MicroRNAs
  • Tretinoin
  • RNA, Long Noncoding
  • TRPM Cation Channels
  • Wnt Proteins
  • MIRN137 microRNA, mouse
  • RNA, Competitive Endogenous