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PEST-containing nuclear protein regulates cell proliferation, migration, and invasion in lung adenocarcinoma
Lung cancer is the leading cause of cancer-related mortality worldwide. PEST-containing nuclear protein (PCNP) has been found in the nucleus of cancer cells. Whether PCNP plays a role in the growth of lung adenocarcinoma is still unknown. In the present study, the results indicated that the level of...
Autores principales: | , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6418141/ https://www.ncbi.nlm.nih.gov/pubmed/30872582 http://dx.doi.org/10.1038/s41389-019-0132-4 |
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author | Wang, Da-Yong Hong, Ya Chen, Ya-Ge Dong, Peng-Zhen Liu, Shi-Yu Gao, Ying-Ran Lu, Dan Li, Hui-Min Li, Tao Guo, Jian-Cheng He, Fei Ren, Xue-Qun Sun, Shi-Yong Wu, Dong-Dong Duan, Shao-Feng Ji, Xin-Ying |
author_facet | Wang, Da-Yong Hong, Ya Chen, Ya-Ge Dong, Peng-Zhen Liu, Shi-Yu Gao, Ying-Ran Lu, Dan Li, Hui-Min Li, Tao Guo, Jian-Cheng He, Fei Ren, Xue-Qun Sun, Shi-Yong Wu, Dong-Dong Duan, Shao-Feng Ji, Xin-Ying |
author_sort | Wang, Da-Yong |
collection | PubMed |
description | Lung cancer is the leading cause of cancer-related mortality worldwide. PEST-containing nuclear protein (PCNP) has been found in the nucleus of cancer cells. Whether PCNP plays a role in the growth of lung adenocarcinoma is still unknown. In the present study, the results indicated that the level of PCNP in lung adenocarcinoma tissue was significantly higher than that in corresponding adjacent non-tumor tissue. Over-expression of PCNP promoted the proliferation, migration, and invasion of lung adenocarcinoma cells, while down-regulation of PCNP exhibited opposite effects. PCNP over-expression decreased apoptosis through up-regulating the expression levels of phospho (p)-signal transducers and activators of transcription (STAT) 3 and p-STAT5 in lung adenocarcinoma cells, whereas PCNP knockdown showed opposite trends. PCNP overexpression enhanced autophagy by increasing the expression levels of p-phosphatidylinositol 3-kinase (PI3K), p-Akt, and p-mammalian target of rapamycin (mTOR) in lung adenocarcinoma cells, however an opposite trend was observed in the sh-PCNP group. In addition, overexpression of PCNP showed the tumor-promoting effect on xenografted lung adenocarcinoma, while PCNP knockdown reduced the growth of lung adenocarcinoma via regulating angiogenesis. Our study elucidates that PCNP can regulate the procession of human lung adenocarcinoma cells via STAT3/5 and PI3K/Akt/mTOR signaling pathways. PCNP may be considered as a promising biomarker for the diagnosis and prognosis in patients with lung adenocarcinoma. Furthermore, PCNP can be a novel therapeutic target and potent PCNP inhibitors can be designed and developed in the treatment of lung adenocarcinoma. |
format | Online Article Text |
id | pubmed-6418141 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-64181412019-03-18 PEST-containing nuclear protein regulates cell proliferation, migration, and invasion in lung adenocarcinoma Wang, Da-Yong Hong, Ya Chen, Ya-Ge Dong, Peng-Zhen Liu, Shi-Yu Gao, Ying-Ran Lu, Dan Li, Hui-Min Li, Tao Guo, Jian-Cheng He, Fei Ren, Xue-Qun Sun, Shi-Yong Wu, Dong-Dong Duan, Shao-Feng Ji, Xin-Ying Oncogenesis Article Lung cancer is the leading cause of cancer-related mortality worldwide. PEST-containing nuclear protein (PCNP) has been found in the nucleus of cancer cells. Whether PCNP plays a role in the growth of lung adenocarcinoma is still unknown. In the present study, the results indicated that the level of PCNP in lung adenocarcinoma tissue was significantly higher than that in corresponding adjacent non-tumor tissue. Over-expression of PCNP promoted the proliferation, migration, and invasion of lung adenocarcinoma cells, while down-regulation of PCNP exhibited opposite effects. PCNP over-expression decreased apoptosis through up-regulating the expression levels of phospho (p)-signal transducers and activators of transcription (STAT) 3 and p-STAT5 in lung adenocarcinoma cells, whereas PCNP knockdown showed opposite trends. PCNP overexpression enhanced autophagy by increasing the expression levels of p-phosphatidylinositol 3-kinase (PI3K), p-Akt, and p-mammalian target of rapamycin (mTOR) in lung adenocarcinoma cells, however an opposite trend was observed in the sh-PCNP group. In addition, overexpression of PCNP showed the tumor-promoting effect on xenografted lung adenocarcinoma, while PCNP knockdown reduced the growth of lung adenocarcinoma via regulating angiogenesis. Our study elucidates that PCNP can regulate the procession of human lung adenocarcinoma cells via STAT3/5 and PI3K/Akt/mTOR signaling pathways. PCNP may be considered as a promising biomarker for the diagnosis and prognosis in patients with lung adenocarcinoma. Furthermore, PCNP can be a novel therapeutic target and potent PCNP inhibitors can be designed and developed in the treatment of lung adenocarcinoma. Nature Publishing Group UK 2019-03-14 /pmc/articles/PMC6418141/ /pubmed/30872582 http://dx.doi.org/10.1038/s41389-019-0132-4 Text en © The Author(s) 2019 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/. |
spellingShingle | Article Wang, Da-Yong Hong, Ya Chen, Ya-Ge Dong, Peng-Zhen Liu, Shi-Yu Gao, Ying-Ran Lu, Dan Li, Hui-Min Li, Tao Guo, Jian-Cheng He, Fei Ren, Xue-Qun Sun, Shi-Yong Wu, Dong-Dong Duan, Shao-Feng Ji, Xin-Ying PEST-containing nuclear protein regulates cell proliferation, migration, and invasion in lung adenocarcinoma |
title | PEST-containing nuclear protein regulates cell proliferation, migration, and invasion in lung adenocarcinoma |
title_full | PEST-containing nuclear protein regulates cell proliferation, migration, and invasion in lung adenocarcinoma |
title_fullStr | PEST-containing nuclear protein regulates cell proliferation, migration, and invasion in lung adenocarcinoma |
title_full_unstemmed | PEST-containing nuclear protein regulates cell proliferation, migration, and invasion in lung adenocarcinoma |
title_short | PEST-containing nuclear protein regulates cell proliferation, migration, and invasion in lung adenocarcinoma |
title_sort | pest-containing nuclear protein regulates cell proliferation, migration, and invasion in lung adenocarcinoma |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6418141/ https://www.ncbi.nlm.nih.gov/pubmed/30872582 http://dx.doi.org/10.1038/s41389-019-0132-4 |
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