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PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway
Some studies have reported that activated ribosomes are positively associated with malignant tumors, especially in hepatocellular carcinoma (HCC). The RNA-binding protein PNO1 is a critical ribosome rarely reported in human tumors. This study aimed to explore the molecular mechanisms of PNO1 in HCC....
Autores principales: | , , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8163843/ https://www.ncbi.nlm.nih.gov/pubmed/34050137 http://dx.doi.org/10.1038/s41419-021-03837-y |
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author | Han, Zhiqiang Liu, Dongming Chen, Lu He, Yuchao Tian, Xiangdong Qi, Lisha Chen, Liwei Luo, Yi Chen, Ziye Hu, Xiaomeng Li, Guangtao Zhan, Linlin Wang, Yu Li, Qiang Chen, Peng Liu, Zhiyong Guo, Hua |
author_facet | Han, Zhiqiang Liu, Dongming Chen, Lu He, Yuchao Tian, Xiangdong Qi, Lisha Chen, Liwei Luo, Yi Chen, Ziye Hu, Xiaomeng Li, Guangtao Zhan, Linlin Wang, Yu Li, Qiang Chen, Peng Liu, Zhiyong Guo, Hua |
author_sort | Han, Zhiqiang |
collection | PubMed |
description | Some studies have reported that activated ribosomes are positively associated with malignant tumors, especially in hepatocellular carcinoma (HCC). The RNA-binding protein PNO1 is a critical ribosome rarely reported in human tumors. This study aimed to explore the molecular mechanisms of PNO1 in HCC. Using 150 formalin-fixed and paraffin-embedded samples and 8 fresh samples, we found high PNO1 expression in HCC tumor tissues through Western blotting and RT-PCR. Moreover, the higher PNO1 expression was associated with poor HCC prognosis patients. In vitro and in vivo experiments indicated that PNO1 overexpression promoted the proliferation and depressed the apoptosis of HCC cells. High PNO1 expression also increased the autophagy of HCC cells. The molecular mechanisms underlying PNO1 were examined by RNA-seq analysis and a series of functional experiments. Results showed that PNO1 promoted HCC progression through the MAPK signaling pathway. Therefore, PNO1 was overexpressed in HCC, promoted autophagy, and inhibited the apoptosis of HCC cells through the MAPK signaling pathway. |
format | Online Article Text |
id | pubmed-8163843 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-81638432021-06-10 PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway Han, Zhiqiang Liu, Dongming Chen, Lu He, Yuchao Tian, Xiangdong Qi, Lisha Chen, Liwei Luo, Yi Chen, Ziye Hu, Xiaomeng Li, Guangtao Zhan, Linlin Wang, Yu Li, Qiang Chen, Peng Liu, Zhiyong Guo, Hua Cell Death Dis Article Some studies have reported that activated ribosomes are positively associated with malignant tumors, especially in hepatocellular carcinoma (HCC). The RNA-binding protein PNO1 is a critical ribosome rarely reported in human tumors. This study aimed to explore the molecular mechanisms of PNO1 in HCC. Using 150 formalin-fixed and paraffin-embedded samples and 8 fresh samples, we found high PNO1 expression in HCC tumor tissues through Western blotting and RT-PCR. Moreover, the higher PNO1 expression was associated with poor HCC prognosis patients. In vitro and in vivo experiments indicated that PNO1 overexpression promoted the proliferation and depressed the apoptosis of HCC cells. High PNO1 expression also increased the autophagy of HCC cells. The molecular mechanisms underlying PNO1 were examined by RNA-seq analysis and a series of functional experiments. Results showed that PNO1 promoted HCC progression through the MAPK signaling pathway. Therefore, PNO1 was overexpressed in HCC, promoted autophagy, and inhibited the apoptosis of HCC cells through the MAPK signaling pathway. Nature Publishing Group UK 2021-05-28 /pmc/articles/PMC8163843/ /pubmed/34050137 http://dx.doi.org/10.1038/s41419-021-03837-y Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/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/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Han, Zhiqiang Liu, Dongming Chen, Lu He, Yuchao Tian, Xiangdong Qi, Lisha Chen, Liwei Luo, Yi Chen, Ziye Hu, Xiaomeng Li, Guangtao Zhan, Linlin Wang, Yu Li, Qiang Chen, Peng Liu, Zhiyong Guo, Hua PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway |
title | PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway |
title_full | PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway |
title_fullStr | PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway |
title_full_unstemmed | PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway |
title_short | PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway |
title_sort | pno1 regulates autophagy and apoptosis of hepatocellular carcinoma via the mapk signaling pathway |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8163843/ https://www.ncbi.nlm.nih.gov/pubmed/34050137 http://dx.doi.org/10.1038/s41419-021-03837-y |
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