학술논문
Silencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
Document Type
Academic Journal
Source
Thoracic Cancer. September 2019, Vol. 10 Issue 9, p1748, 16 p.
Subject
Language
English
ISSN
1759-7706
Abstract
Introduction Lung cancer currently ranks as the leading cause of cancer‐related mortality in men and the second leading cause in women throughout the world, with variations in its incidence and [...]
Background: 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. Methods: 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. Results: 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. Conclusion: 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.
Background: 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. Methods: 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. Results: 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. Conclusion: 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.