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. 2021 Aug 13;9:714787. doi: 10.3389/fcell.2021.714787

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Copyright © 2021 Ghafouri-Fard, Azimi, Hussen, Abak, Taheri and Dilmaghani.

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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A schematic representation of the crosstalk between Hippo signaling cascade and lncRNA NORAD in lung and breast neoplasms. YAP/TAZ is mainly modulated via the canonical Hippo cascade, MST1/2-SAV1, and LATS1/2-MOB1. LATS1/2 could in turn phosphorylate YAP/TAZ and suppress its function through either ubiquitination and proteasome-mediated degradation or 14-3-3-mediated cytoplasmic sequestration. Unphosphorylated YAP/TAZ is transferred to the nucleus, where it could interact with TEAD transcription factors and trigger the expression of various target genes. LATS1/2 could be upregulated via STK25, TAOK, NF2, and MAP4KS, while being inhibited through GPCR-RHOA-mediated F-actin function mechanical cues as well as NUAK2. In addition, expression of MST1/2 is regulated by TAOK and MARK4. Expression of YAP/TAZ is also modulated in an independent manner from LATS. Besides, PTPN14 and AMOT could interact with YAP/TAZ and sequester it in the cell membrane. Expression of YAP/TAZ is downregulated via the β-catenin demolition complex or TIAM1 through a direct interaction. Phosphorylation of YAP/TAZ is triggered by CDK1, AMPK, Aurora A, NLK, and various RTKs. In addition, p38 and VGLL4 could interact with TEAD and inhibit the function of YAP/TAZ (Yamaguchi and Taouk, 2020). Mounting evidence has collectively demonstrated that the Hippo pathway transducer YAP/TAZ-TEAD complex could play an effective role in suppressing the expression level of lncRNA NORAD in both lung and breast cancers. Its downregulation correlates with enhancement of migration, invasion as well as metastasis in tumor cells (Tan et al., 2019).