author_facet Wu, Yuanyuan
Wang, Huifeng
Qiao, Lijiao
Jin, Xiangming
Dong, Hui
Wang, Yan
Wu, Yuanyuan
Wang, Huifeng
Qiao, Lijiao
Jin, Xiangming
Dong, Hui
Wang, Yan
author Wu, Yuanyuan
Wang, Huifeng
Qiao, Lijiao
Jin, Xiangming
Dong, Hui
Wang, Yan
spellingShingle Wu, Yuanyuan
Wang, Huifeng
Qiao, Lijiao
Jin, Xiangming
Dong, Hui
Wang, Yan
Thoracic Cancer
Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
Pulmonary and Respiratory Medicine
Oncology
General Medicine
author_sort wu, yuanyuan
spelling Wu, Yuanyuan Wang, Huifeng Qiao, Lijiao Jin, Xiangming Dong, Hui Wang, Yan 1759-7706 1759-7714 Wiley Pulmonary and Respiratory Medicine Oncology General Medicine http://dx.doi.org/10.1111/1759-7714.13124 <jats:sec><jats:title>Background</jats:title><jats:p>Non‐small cell lung cancer (NSCLC) is a major cause of cancer‐related mortality and is frequently accompanied by metastasis. The crucial roles of genes in lung cancer have attracted attention. Thus, this study aimed to investigate the effects of RAD51AP1 on the epithelial–mesenchymal transition (EMT) and metastasis of NSCLC.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>The positive expression rate of the RAD51AP1 protein was examined. NSCLC cells were transfected with a series of plasmids to alter the expression of RAD51AP1 to clarify the influence of RAD51AP1 on EMT and metastasis in NSCLC, as well as NSCLC cell migration, invasion, apoptosis, proliferation, and cloning. An in vivo experiment was conducted to determine the oncogenicity of human NSCLC cells in nude mice.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>RAD51AP1 was highly expressed in NSCLC tissues. Furthermore, we found promotion of N‐cadherin, vimentin, fibronectin, MMP‐2, OPN, CD62, and TMP‐2, but inhibition of E‐cadherin, occludin, cytokeratin in the context of elevated RAD51AP1 expression. An in vivo experiment also confirmed that silencing of RAD51AP1 could inhibit NSCLC tumor formation and growth.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Our results revealed that RAD51AP1 silencing suppressed the EMT and metastasis of NSCLC, thereby highlighting its potential as a promising novel target for NSCLC treatment.</jats:p></jats:sec> Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer Thoracic Cancer
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title Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
title_unstemmed Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
title_full Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
title_fullStr Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
title_full_unstemmed Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
title_short Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
title_sort silencing of rad51ap1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
topic Pulmonary and Respiratory Medicine
Oncology
General Medicine
url http://dx.doi.org/10.1111/1759-7714.13124
publishDate 2019
physical 1748-1763
description <jats:sec><jats:title>Background</jats:title><jats:p>Non‐small cell lung cancer (NSCLC) is a major cause of cancer‐related mortality and is frequently accompanied by metastasis. The crucial roles of genes in lung cancer have attracted attention. Thus, this study aimed to investigate the effects of RAD51AP1 on the epithelial–mesenchymal transition (EMT) and metastasis of NSCLC.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>The positive expression rate of the RAD51AP1 protein was examined. NSCLC cells were transfected with a series of plasmids to alter the expression of RAD51AP1 to clarify the influence of RAD51AP1 on EMT and metastasis in NSCLC, as well as NSCLC cell migration, invasion, apoptosis, proliferation, and cloning. An in vivo experiment was conducted to determine the oncogenicity of human NSCLC cells in nude mice.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>RAD51AP1 was highly expressed in NSCLC tissues. Furthermore, we found promotion of N‐cadherin, vimentin, fibronectin, MMP‐2, OPN, CD62, and TMP‐2, but inhibition of E‐cadherin, occludin, cytokeratin in the context of elevated RAD51AP1 expression. An in vivo experiment also confirmed that silencing of RAD51AP1 could inhibit NSCLC tumor formation and growth.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Our results revealed that RAD51AP1 silencing suppressed the EMT and metastasis of NSCLC, thereby highlighting its potential as a promising novel target for NSCLC treatment.</jats:p></jats:sec>
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author Wu, Yuanyuan, Wang, Huifeng, Qiao, Lijiao, Jin, Xiangming, Dong, Hui, Wang, Yan
author_facet Wu, Yuanyuan, Wang, Huifeng, Qiao, Lijiao, Jin, Xiangming, Dong, Hui, Wang, Yan, Wu, Yuanyuan, Wang, Huifeng, Qiao, Lijiao, Jin, Xiangming, Dong, Hui, Wang, Yan
author_sort wu, yuanyuan
container_issue 9
container_start_page 1748
container_title Thoracic Cancer
container_volume 10
description <jats:sec><jats:title>Background</jats:title><jats:p>Non‐small cell lung cancer (NSCLC) is a major cause of cancer‐related mortality and is frequently accompanied by metastasis. The crucial roles of genes in lung cancer have attracted attention. Thus, this study aimed to investigate the effects of RAD51AP1 on the epithelial–mesenchymal transition (EMT) and metastasis of NSCLC.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>The positive expression rate of the RAD51AP1 protein was examined. NSCLC cells were transfected with a series of plasmids to alter the expression of RAD51AP1 to clarify the influence of RAD51AP1 on EMT and metastasis in NSCLC, as well as NSCLC cell migration, invasion, apoptosis, proliferation, and cloning. An in vivo experiment was conducted to determine the oncogenicity of human NSCLC cells in nude mice.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>RAD51AP1 was highly expressed in NSCLC tissues. Furthermore, we found promotion of N‐cadherin, vimentin, fibronectin, MMP‐2, OPN, CD62, and TMP‐2, but inhibition of E‐cadherin, occludin, cytokeratin in the context of elevated RAD51AP1 expression. An in vivo experiment also confirmed that silencing of RAD51AP1 could inhibit NSCLC tumor formation and growth.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Our results revealed that RAD51AP1 silencing suppressed the EMT and metastasis of NSCLC, thereby highlighting its potential as a promising novel target for NSCLC treatment.</jats:p></jats:sec>
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spelling Wu, Yuanyuan Wang, Huifeng Qiao, Lijiao Jin, Xiangming Dong, Hui Wang, Yan 1759-7706 1759-7714 Wiley Pulmonary and Respiratory Medicine Oncology General Medicine http://dx.doi.org/10.1111/1759-7714.13124 <jats:sec><jats:title>Background</jats:title><jats:p>Non‐small cell lung cancer (NSCLC) is a major cause of cancer‐related mortality and is frequently accompanied by metastasis. The crucial roles of genes in lung cancer have attracted attention. Thus, this study aimed to investigate the effects of RAD51AP1 on the epithelial–mesenchymal transition (EMT) and metastasis of NSCLC.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>The positive expression rate of the RAD51AP1 protein was examined. NSCLC cells were transfected with a series of plasmids to alter the expression of RAD51AP1 to clarify the influence of RAD51AP1 on EMT and metastasis in NSCLC, as well as NSCLC cell migration, invasion, apoptosis, proliferation, and cloning. An in vivo experiment was conducted to determine the oncogenicity of human NSCLC cells in nude mice.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>RAD51AP1 was highly expressed in NSCLC tissues. Furthermore, we found promotion of N‐cadherin, vimentin, fibronectin, MMP‐2, OPN, CD62, and TMP‐2, but inhibition of E‐cadherin, occludin, cytokeratin in the context of elevated RAD51AP1 expression. An in vivo experiment also confirmed that silencing of RAD51AP1 could inhibit NSCLC tumor formation and growth.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Our results revealed that RAD51AP1 silencing suppressed the EMT and metastasis of NSCLC, thereby highlighting its potential as a promising novel target for NSCLC treatment.</jats:p></jats:sec> Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer Thoracic Cancer
spellingShingle Wu, Yuanyuan, Wang, Huifeng, Qiao, Lijiao, Jin, Xiangming, Dong, Hui, Wang, Yan, Thoracic Cancer, Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer, Pulmonary and Respiratory Medicine, Oncology, General Medicine
title Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
title_full Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
title_fullStr Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
title_full_unstemmed Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
title_short Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
title_sort silencing of rad51ap1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
title_unstemmed Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
topic Pulmonary and Respiratory Medicine, Oncology, General Medicine
url http://dx.doi.org/10.1111/1759-7714.13124