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. 2021 Jun 5;12(6):581. doi: 10.1038/s41419-021-03871-w

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© The Author(s) 2021

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. 7 — A Pirh2 stimulates proliferation of H1299 cells. Cell index graphs demonstrating the proliferation registered by xCelligence system for H1299 cells with stable Pirh2 overexpression (Pirh2 OE) and control H1299 cells (ctrl). B Pirh2 knockdown suppresses proliferation of H1299 cells. Cell index graphs registered by xCelligence system for H1299 cells with stable Pirh2 knockdown (Pirh2 KD) and control H1299 cells (scrambled). C The bioinformatics analysis of the effect of simultaneous rchy1 and myc genes (coding Pirh2 and c-Myc, respectively), and elavl1 gene (coding HuR protein) expression on lung adenocarcinoma patients’ (GEO dataset ID: GSE31210) survival probability. P-values are indicated. D Graphical scheme summarizing the role of Pirh2 in HuR protein stability regulation. Pirh2 ubiquitinates HuR that leads to HuR proteasomal degradation and influence on HuR target mRNA stability.