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. 2022 Feb 18;29(10):1307–1320. doi: 10.1038/s41417-022-00434-9

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Fus1/Tusc2 gene is regulated on transcriptional level by different physiological and pathological factors such as ROS, hypoxia, and differentiation molecules (e.g., RANKL). In some tumors (e.g., NSCLC), DNA methylation may lead to down-regulation of TUSC2 gene transcription. Binding of microRNAs (miRs) to 3’ and 5’ untranslated regions (UTR) of TUSC2 mRNA suppresses its translation. mRNA for TUSC2 pseudogene (TUSC2P) sequesters miRNAs and prevents their binding to TUSC2 mRNA. During translation, 5’ UTR can adopt conformation preferring stoppage of ribosomes along TUSC2 mRNA observed in NSCLC tumor cells. After effective translation, Fus1/Tusc2 undergoes myristoylation (Myr) which is necessary for a protein stability in normal cells; in the absence of Myr tail (in tumor cells), protein is degraded at faster rate via proteasome machinery.