Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway
BACKGROUND: Zinc finger protein 687 (ZNF687) has previously been discovered as a potential oncogene in individuals with giant cell tumors of the bone, acute myeloid leukemia, and hepatocellular carcinoma. However, its role and mechanism in lung adenocarcinoma (LUAD) remain unclear. METHODS: In LUAD...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley & Sons Australia, Ltd
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10175037/ https://www.ncbi.nlm.nih.gov/pubmed/36944484 http://dx.doi.org/10.1111/1759-7714.14856 |
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author | Li, Mingchun Liu, Zhihua Hou, Zan Wang, Xiangcai Shi, Huaqiu Li, Yamei Xiao, Xuewen Tang, Zhixian Yang, Jianqiong Luo, Yaoling Zhang, Minhong Chen, Ming |
author_facet | Li, Mingchun Liu, Zhihua Hou, Zan Wang, Xiangcai Shi, Huaqiu Li, Yamei Xiao, Xuewen Tang, Zhixian Yang, Jianqiong Luo, Yaoling Zhang, Minhong Chen, Ming |
author_sort | Li, Mingchun |
collection | PubMed |
description | BACKGROUND: Zinc finger protein 687 (ZNF687) has previously been discovered as a potential oncogene in individuals with giant cell tumors of the bone, acute myeloid leukemia, and hepatocellular carcinoma. However, its role and mechanism in lung adenocarcinoma (LUAD) remain unclear. METHODS: In LUAD cells, tumor, and matched adjacent tissue specimens, quantitative real‐time RT‐ polymerase chain reaction (qRT‐PCR), western blotting analyses, and immunohistochemistry staining (IHC) were conducted. Cell counting kit‐8 (CCK8) assay, clonogenicity analysis, flow cytometry, and transwell assays were utilized to detect ZNF687 overexpression and knockdown impacts on cell growth, colony formation, cell cycle, migration, and invasion. Bioinformatic studies, qRT‐PCR and western blotting studies were employed to validate the underlying mechanisms and signaling pathways implicated in the oncogenic effect of ZNF687. RESULTS: This study demonstrated that ZNF687 expression was elevated in LUAD cells and tissues. Individuals with upregulated ZNF687 had a poorer prognosis than those with downregulatedZNF687 (p < 0.001). ZNF687 overexpression enhanced LUAD growth, migration, invasion and colony formation, and the cell cycle G1‐S transition; additionally, it promoted the epithelial‐mesenchymal transition (EMT). In contrast, knocking down ZNF687 showed to have the opposite impact. Moreover, these effects were associated with the activity of the phosphatidylinositol 3‐kinase (PI3K)/protein kinase B (AKT) signaling mechanism. CONCLUSION: ZNF687 was upregulated in LUAD, and high ZNF687 expression levels are associated with poor prognoses. The activation of the PI3K/AKT signaling pathway by upregulated ZNF687 increased the proliferation of LUAD cells and tumor progression. ZNF687 may be a beneficial predictive marker and a therapeutic target in LUAD. |
format | Online Article Text |
id | pubmed-10175037 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley & Sons Australia, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-101750372023-05-12 Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway Li, Mingchun Liu, Zhihua Hou, Zan Wang, Xiangcai Shi, Huaqiu Li, Yamei Xiao, Xuewen Tang, Zhixian Yang, Jianqiong Luo, Yaoling Zhang, Minhong Chen, Ming Thorac Cancer Original Articles BACKGROUND: Zinc finger protein 687 (ZNF687) has previously been discovered as a potential oncogene in individuals with giant cell tumors of the bone, acute myeloid leukemia, and hepatocellular carcinoma. However, its role and mechanism in lung adenocarcinoma (LUAD) remain unclear. METHODS: In LUAD cells, tumor, and matched adjacent tissue specimens, quantitative real‐time RT‐ polymerase chain reaction (qRT‐PCR), western blotting analyses, and immunohistochemistry staining (IHC) were conducted. Cell counting kit‐8 (CCK8) assay, clonogenicity analysis, flow cytometry, and transwell assays were utilized to detect ZNF687 overexpression and knockdown impacts on cell growth, colony formation, cell cycle, migration, and invasion. Bioinformatic studies, qRT‐PCR and western blotting studies were employed to validate the underlying mechanisms and signaling pathways implicated in the oncogenic effect of ZNF687. RESULTS: This study demonstrated that ZNF687 expression was elevated in LUAD cells and tissues. Individuals with upregulated ZNF687 had a poorer prognosis than those with downregulatedZNF687 (p < 0.001). ZNF687 overexpression enhanced LUAD growth, migration, invasion and colony formation, and the cell cycle G1‐S transition; additionally, it promoted the epithelial‐mesenchymal transition (EMT). In contrast, knocking down ZNF687 showed to have the opposite impact. Moreover, these effects were associated with the activity of the phosphatidylinositol 3‐kinase (PI3K)/protein kinase B (AKT) signaling mechanism. CONCLUSION: ZNF687 was upregulated in LUAD, and high ZNF687 expression levels are associated with poor prognoses. The activation of the PI3K/AKT signaling pathway by upregulated ZNF687 increased the proliferation of LUAD cells and tumor progression. ZNF687 may be a beneficial predictive marker and a therapeutic target in LUAD. John Wiley & Sons Australia, Ltd 2023-03-21 /pmc/articles/PMC10175037/ /pubmed/36944484 http://dx.doi.org/10.1111/1759-7714.14856 Text en © 2023 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Li, Mingchun Liu, Zhihua Hou, Zan Wang, Xiangcai Shi, Huaqiu Li, Yamei Xiao, Xuewen Tang, Zhixian Yang, Jianqiong Luo, Yaoling Zhang, Minhong Chen, Ming Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway |
title | Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway |
title_full | Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway |
title_fullStr | Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway |
title_full_unstemmed | Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway |
title_short | Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway |
title_sort | oncogenic zinc finger protein znf687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the pi3k/akt signaling pathway |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10175037/ https://www.ncbi.nlm.nih.gov/pubmed/36944484 http://dx.doi.org/10.1111/1759-7714.14856 |
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