1. The role of lncRNA Meg3 in the proliferation of all-trans retinoic acid-treated mouse embryonic palate mesenchymal cells involves the Smad pathway.
- Author
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Liu X, Liu H, Wu Y, He Z, Shen L, Zhang H, Wan Z, Chen Y, Yue H, Zhang T, Gao S, and Yu Z
- Subjects
- Animals, Cells, Cultured, Cleft Palate, Gene Expression Regulation, Developmental, Mesenchymal Stem Cells, Mice, Palate, Phosphorylation, Signal Transduction, Transforming Growth Factor beta3, Cell Proliferation physiology, RNA, Long Noncoding, Tretinoin toxicity
- Abstract
Mesenchymal cell proliferation is critical for the growth of the palate shelf. All-trans retinoic acid (atRA), as well as pathways associated with TGF-β/Smad signaling, play crucial roles in the proliferation of mouse embryonic palate mesenchymal (MEPM) cells. We have found that MEPM-cell proliferation was regulated by atRA and exogenous TGF-β3 could significantly antagonize the atRA-mediated suppression of MEPM cell proliferation, which is closely associated with the regulation of TGF-β/Smad signaling pathway. The long non-coding RNA (lncRNA) MEG3 has been reported to activate TGF-β/Smad signaling, thereby regulating cellular proliferation, differentiation, and related processes. Here, we found that Meg3 expression increased significantly in atRA-treated MEPM cells while TGF-β3 treatment markedly inhibited Meg3 expression and antagonized the effect of atRA on Meg3. Moreover, Smad2 was found to interact directly with Meg3, and atRA treatment significantly enriched Meg3 in Smad2-immunoprecipitated samples. After Meg3 deletion, the effects of atRA on the proliferation of MEPM cells and TGF-β3-dependent protein expression were lost. Hence, we speculate that Meg3 has a role in the RA-induced suppression of MEPM cell proliferation by targeting Smad2 and thereby mediating TGF-β/Smad signaling inhibition., (Copyright © 2021 Elsevier Inc. All rights reserved.)
- Published
- 2021
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