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
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 o...
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Veröffentlicht in: | Environmental toxicology and pharmacology 2024-12, p.104623, Article 104623 |
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Zusammenfassung: | 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.
•Long non-coding RNAs and microRNAs regulated genes controlling cleft palate formation•Constructed a lncRNA-miRNA-mRNA ceRNA regulatory network by predicting ceRNAs•ENSMUST00000159153-miR-137-5p-Wnt7a may be critical in cleft palate formation•ENSMUST00000236086-miR-34b-3p-EphA10/TRPM2 may be important in causing cleft palate |
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ISSN: | 1382-6689 1872-7077 1872-7077 |
DOI: | 10.1016/j.etap.2024.104623 |