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ANKRD49 promotes the invasion and metastasis of lung adenocarcinoma via a P38/ATF‐2 signalling pathway
Lung adenocarcinoma (LUAD) is the most challenging neoplasm to treat in clinical practice. Ankyrin repeat domain 49 protein (ANKRD49) is highly expressed in several carcinomas; however, its pattern of expression and role in LUAD are not known. Tissue microarrays, immunohistochemistry, χ (2) test, Sp...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9357638/ https://www.ncbi.nlm.nih.gov/pubmed/35775112 http://dx.doi.org/10.1111/jcmm.17464 |
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author | Liu, Yue‐hua Yuan, Meng Xu, Bai‐xue Gao, Rui You, Yu‐jie Wang, Zhi‐xin Zhang, Yong‐cai Guo, Min Chen, Zhao‐yang Yu, Bao‐feng Wang, Qi‐Wei Wang, Hai‐long Pang, Min |
author_facet | Liu, Yue‐hua Yuan, Meng Xu, Bai‐xue Gao, Rui You, Yu‐jie Wang, Zhi‐xin Zhang, Yong‐cai Guo, Min Chen, Zhao‐yang Yu, Bao‐feng Wang, Qi‐Wei Wang, Hai‐long Pang, Min |
author_sort | Liu, Yue‐hua |
collection | PubMed |
description | Lung adenocarcinoma (LUAD) is the most challenging neoplasm to treat in clinical practice. Ankyrin repeat domain 49 protein (ANKRD49) is highly expressed in several carcinomas; however, its pattern of expression and role in LUAD are not known. Tissue microarrays, immunohistochemistry, χ (2) test, Spearman correlation analysis, Kaplan–Meier, log‐rank test, and Cox's proportional hazard model were used to analyse the clinical cases. The effect of ANKRD49 on the LUAD was investigated using CCK‐8, clonal formation, would healing, transwell assays, and nude mice experiment. Expressions of ANKRD49 and its associated downstream protein molecules were verified by real‐time PCR, Western blot, immunohistochemistry, and/or immunofluorescence analyses. ANKRD49 expression was highly elevated in LUAD. The survival rate and Cox's modelling analysis indicated that there may be an independent prognostic indicator for LUAD patients. We also found that ANKRD49 promoted the invasion and migration in both in in vitro and in vivo assays, through upregulating matrix metalloproteinase (MMP)‐2 and MMP‐9 activities via the P38/ATF‐2 signalling pathway Our findings suggest that ANKRD49 is a latent biomarker for evaluating LUAD prognosis and promotes the metastasis of A549 cells via upregulation of MMP‐2 and MMP‐9 in a P38/ATF‐2 pathway‐dependent manner. |
format | Online Article Text |
id | pubmed-9357638 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-93576382022-08-09 ANKRD49 promotes the invasion and metastasis of lung adenocarcinoma via a P38/ATF‐2 signalling pathway Liu, Yue‐hua Yuan, Meng Xu, Bai‐xue Gao, Rui You, Yu‐jie Wang, Zhi‐xin Zhang, Yong‐cai Guo, Min Chen, Zhao‐yang Yu, Bao‐feng Wang, Qi‐Wei Wang, Hai‐long Pang, Min J Cell Mol Med Original Articles Lung adenocarcinoma (LUAD) is the most challenging neoplasm to treat in clinical practice. Ankyrin repeat domain 49 protein (ANKRD49) is highly expressed in several carcinomas; however, its pattern of expression and role in LUAD are not known. Tissue microarrays, immunohistochemistry, χ (2) test, Spearman correlation analysis, Kaplan–Meier, log‐rank test, and Cox's proportional hazard model were used to analyse the clinical cases. The effect of ANKRD49 on the LUAD was investigated using CCK‐8, clonal formation, would healing, transwell assays, and nude mice experiment. Expressions of ANKRD49 and its associated downstream protein molecules were verified by real‐time PCR, Western blot, immunohistochemistry, and/or immunofluorescence analyses. ANKRD49 expression was highly elevated in LUAD. The survival rate and Cox's modelling analysis indicated that there may be an independent prognostic indicator for LUAD patients. We also found that ANKRD49 promoted the invasion and migration in both in in vitro and in vivo assays, through upregulating matrix metalloproteinase (MMP)‐2 and MMP‐9 activities via the P38/ATF‐2 signalling pathway Our findings suggest that ANKRD49 is a latent biomarker for evaluating LUAD prognosis and promotes the metastasis of A549 cells via upregulation of MMP‐2 and MMP‐9 in a P38/ATF‐2 pathway‐dependent manner. John Wiley and Sons Inc. 2022-06-30 2022-08 /pmc/articles/PMC9357638/ /pubmed/35775112 http://dx.doi.org/10.1111/jcmm.17464 Text en © 2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons 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 Liu, Yue‐hua Yuan, Meng Xu, Bai‐xue Gao, Rui You, Yu‐jie Wang, Zhi‐xin Zhang, Yong‐cai Guo, Min Chen, Zhao‐yang Yu, Bao‐feng Wang, Qi‐Wei Wang, Hai‐long Pang, Min ANKRD49 promotes the invasion and metastasis of lung adenocarcinoma via a P38/ATF‐2 signalling pathway |
title |
ANKRD49 promotes the invasion and metastasis of lung adenocarcinoma via a P38/ATF‐2 signalling pathway |
title_full |
ANKRD49 promotes the invasion and metastasis of lung adenocarcinoma via a P38/ATF‐2 signalling pathway |
title_fullStr |
ANKRD49 promotes the invasion and metastasis of lung adenocarcinoma via a P38/ATF‐2 signalling pathway |
title_full_unstemmed |
ANKRD49 promotes the invasion and metastasis of lung adenocarcinoma via a P38/ATF‐2 signalling pathway |
title_short |
ANKRD49 promotes the invasion and metastasis of lung adenocarcinoma via a P38/ATF‐2 signalling pathway |
title_sort | ankrd49 promotes the invasion and metastasis of lung adenocarcinoma via a p38/atf‐2 signalling pathway |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9357638/ https://www.ncbi.nlm.nih.gov/pubmed/35775112 http://dx.doi.org/10.1111/jcmm.17464 |
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