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. 2023 Jun 13;11:1164301. doi: 10.3389/fcell.2023.1164301

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Copyright © 2023 Baba, Baba, Mir, Elfaki, Algehainy, Ullah, Barnawi, Altemani, Alanazi, Mustafa, Masoodi, Akil, Bhat and Macha.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematics showing pathways modulated by lncRNAs to induce EMT. (A) Interaction of TGF-β ligands with T-βR triggers the canonical TGF-pathway, leading to the formation of trimeric SMAD complexes (SMAD2–SMAD3–SMAD4) which act as transcription factors in the nucleus to regulate the expression of EMT-associated genes. lncRNAs, such as LINC00978 and TUG1, can modulate the TGF-β/SMAD signaling transduction by affecting the expression and phosphorylation of SMAD2/3 and SMAD4, respectively. (B) Interaction of Wnt ligands with frizzled receptors triggers the canonical Wnt pathway, leading to the release of β-catenin which binds with LEF and TCF to promote the expression of EMT-related genes. lncRNAs AFAP1-AS1 and HOTAIR modulate the Wnt/β-catenin pathway by affecting the phosphorylation of GSK3β and methylation of H3K27, respectively. (C) Interaction of Jagged/Delta-like ligands with Notch receptors triggers the canonical Notch pathway, leading to the generation of NICD which acts as a transcriptional co-activator in the nucleus. lncRNAs HNF1A-AS1 and UCA1 modulate the Notch pathway by regulating the expression of essential components and acting as ceRNA to regulate Notch signaling indirectly. (D) Growth factors activating the MEK-ERK and PI3K-AKT pathways also induce EMT through simultaneous activation of EMT-TFs. lncRNAs, such as UCA1 and HOXA-AS3, can act as ceRNA to regulate the expression of CREB1 and miR-29c, by promoting PIK3/AKT/mTOR pathway, and enhance the phosphorylation of MEK and ERK, respectively.