Open AccessSilencing of RAD51AP1 suppresses epithelial–mesenchymal transition and metastasis in non‐small cell lung cancer
Author(s) -
Wu Yuanyuan,
Wang Huifeng,
Qiao Lijiao,
Jin Xiangming,
Dong Hui,
Wang Yan
Publication year - 2019
Publication title -
thoracic cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 28
eISSN - 1759-7714
pISSN - 1759-7706
DOI - 10.1111/1759-7714.13124
Subject(s) - gene silencing , epithelial–mesenchymal transition , metastasis , cancer research , vimentin , lung cancer , medicine , cytokeratin , context (archaeology) , transfection , cancer , oncology , pathology , biology , cell culture , immunohistochemistry , gene , paleontology , biochemistry , genetics
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.