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YRDC is upregulated in non-small cell lung cancer and promotes cell proliferation by decreasing cell apoptosis
Non-small cell lung cancer (NSCLC) is the leading cause of cancer-associated mortality worldwide. yrdC N6-threonylcarbamoltransferase domain containing protein (YRDC) has been demonstrated to be involved in the formation of threonylcarbamoyladenosine in transfer ribonucleic acid. However, the molecu...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7285791/ https://www.ncbi.nlm.nih.gov/pubmed/32565932 http://dx.doi.org/10.3892/ol.2020.11560 |
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author | Shen, Haibo Zheng, Enkuo Yang, Zhenhua Yang, Minglei Xu, Xiang Zhou, Yinjie Ni, Junjun Li, Rui Zhao, Guofang |
author_facet | Shen, Haibo Zheng, Enkuo Yang, Zhenhua Yang, Minglei Xu, Xiang Zhou, Yinjie Ni, Junjun Li, Rui Zhao, Guofang |
author_sort | Shen, Haibo |
collection | PubMed |
description | Non-small cell lung cancer (NSCLC) is the leading cause of cancer-associated mortality worldwide. yrdC N6-threonylcarbamoltransferase domain containing protein (YRDC) has been demonstrated to be involved in the formation of threonylcarbamoyladenosine in transfer ribonucleic acid. However, the molecular mechanisms underlying NSCLC progression remain largely unclear. The present study revealed that YRDC was upregulated in NSCLC samples compared with adjacent non-cancerous tissues by analyzing datasets obtained from the Gene Expression Omnibus and The Cancer Genome Atlas. Higher expression of YRDC was associated with overall survival time and disease-free survival time in patients with NSCLC, particularly in lung adenocarcinoma. Furthermore, knockdown of YRDC in NSCLS cell lines significantly suppressed cell growth and cell colony formation in vitro. Additionally, the results demonstrated that silencing of YRDC induced apoptosis of A549 cells. Then, the protein-protein interaction networks associated with yrdC N6-threonylcarbamoltransferase domain containing protein (YRDC) in NSCLC were subsequently constructed to investigate the potential molecular mechanism underlying the role of YRDC in NSCLC. The results revealed that YRDC was involved in the regulation of spliceosomes, ribosomes, the p53 signaling pathway, proteasomes, the cell cycle and DNA replication. The present study demonstrated that YRDC may serve as a novel biomarker for the prognosis prediction and treatment of NSCLC. |
format | Online Article Text |
id | pubmed-7285791 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-72857912020-06-18 YRDC is upregulated in non-small cell lung cancer and promotes cell proliferation by decreasing cell apoptosis Shen, Haibo Zheng, Enkuo Yang, Zhenhua Yang, Minglei Xu, Xiang Zhou, Yinjie Ni, Junjun Li, Rui Zhao, Guofang Oncol Lett Articles Non-small cell lung cancer (NSCLC) is the leading cause of cancer-associated mortality worldwide. yrdC N6-threonylcarbamoltransferase domain containing protein (YRDC) has been demonstrated to be involved in the formation of threonylcarbamoyladenosine in transfer ribonucleic acid. However, the molecular mechanisms underlying NSCLC progression remain largely unclear. The present study revealed that YRDC was upregulated in NSCLC samples compared with adjacent non-cancerous tissues by analyzing datasets obtained from the Gene Expression Omnibus and The Cancer Genome Atlas. Higher expression of YRDC was associated with overall survival time and disease-free survival time in patients with NSCLC, particularly in lung adenocarcinoma. Furthermore, knockdown of YRDC in NSCLS cell lines significantly suppressed cell growth and cell colony formation in vitro. Additionally, the results demonstrated that silencing of YRDC induced apoptosis of A549 cells. Then, the protein-protein interaction networks associated with yrdC N6-threonylcarbamoltransferase domain containing protein (YRDC) in NSCLC were subsequently constructed to investigate the potential molecular mechanism underlying the role of YRDC in NSCLC. The results revealed that YRDC was involved in the regulation of spliceosomes, ribosomes, the p53 signaling pathway, proteasomes, the cell cycle and DNA replication. The present study demonstrated that YRDC may serve as a novel biomarker for the prognosis prediction and treatment of NSCLC. D.A. Spandidos 2020-07 2020-04-21 /pmc/articles/PMC7285791/ /pubmed/32565932 http://dx.doi.org/10.3892/ol.2020.11560 Text en Copyright: © Shen et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Shen, Haibo Zheng, Enkuo Yang, Zhenhua Yang, Minglei Xu, Xiang Zhou, Yinjie Ni, Junjun Li, Rui Zhao, Guofang YRDC is upregulated in non-small cell lung cancer and promotes cell proliferation by decreasing cell apoptosis |
title | YRDC is upregulated in non-small cell lung cancer and promotes cell proliferation by decreasing cell apoptosis |
title_full | YRDC is upregulated in non-small cell lung cancer and promotes cell proliferation by decreasing cell apoptosis |
title_fullStr | YRDC is upregulated in non-small cell lung cancer and promotes cell proliferation by decreasing cell apoptosis |
title_full_unstemmed | YRDC is upregulated in non-small cell lung cancer and promotes cell proliferation by decreasing cell apoptosis |
title_short | YRDC is upregulated in non-small cell lung cancer and promotes cell proliferation by decreasing cell apoptosis |
title_sort | yrdc is upregulated in non-small cell lung cancer and promotes cell proliferation by decreasing cell apoptosis |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7285791/ https://www.ncbi.nlm.nih.gov/pubmed/32565932 http://dx.doi.org/10.3892/ol.2020.11560 |
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