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Silencing of RAD51AP1 suppresses epithelial-mesenchymal transition and metastasis in non-small cell lung cancer.

ABSTRACT: 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.

SUBMITTER: Wu Y

PROVIDER: S-EPMC6718026 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

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Silencing of RAD51AP1 suppresses epithelial-mesenchymal transition and metastasis in non-small cell lung cancer.

Wu Yuanyuan Y Wang Huifeng H Qiao Lijiao L Jin Xiangming X Dong Hui H Wang Yan Y

Thoracic cancer 20190717 9

<h4>Background</h4>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.<h4>Methods</h4>The positive expression rate of the RAD51AP1 protein was examined. NSCLC cells were transfected with a series of plasmids to alter the expr ...[more]

PMID: 31317661

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Project description:Background: Dysregulation of microRNAs (miRNAs) is associated with the pathogenesis of non-small cell lung cancer (NSCLC). However, the mechanisms through which miR-182-5p regulate NSCLC progression have not been established. This study aimed at evaluating the expression levels of miR-182-5p in human NSCLC and its function in lung cancer cells. Endothelial PAS Domain-containing protein 1 (EPAS1; also referred to as hypoxia-inducing factor 2A, HIF-2α) is a transcription factor that is responsible for induction of genes related to cell survival under hypoxia conditions. Hypoxia, an inherent feature of solid tumors, is associated with aggressive phenotypes, as well as resistance to radiotherapy and chemotherapy, which predict metastasis and poor prognosis. Methods: The Cancer Genome Atlas (TCGA) dataset was used to investigate the association between miR-182-5p expression and clinicopathological characteristics as well as prognosis of NSCLC patients. Target genes of miR-182-5p were identified using the PITA, miRmap, microT, miRanda, PicTar, and TargetScan prediction tools. Transwell assays were performed to determine the potential functions of miR-182-5p in lung cancer cells. Luciferase reporter assays were performed to analyze regulation of the putative target of miR-182-5p while western blot assays were used to validate the luciferase results. Results: miR-182-5p was found to be upregulated in NSCLC tissues and acted as an independent prognostic factor for tumor recurrence in NSCLC patients. Functionally, overexpression of miR-182-5p promoted lung cancer cell migration and invasion. Genome-wide gene expression analysis and luciferase report assays revealed that EPAS1 is a direct target of miR-182-5p. EPAS1 was negatively correlated with miR-182-5p expression in NSCLC tissues. Univariate and multivariate survival analyses identified EPAS1 as an independent prognostic factor for overall survival (OS) in NSCLC. Conclusions: These findings imply that miR-182-5p promotes NSCLC progression by targeting EPAS1 and is, therefore, a potential indicator of tumor recurrence in NSCLC patients.

Dataset Information

Silencing of RAD51AP1 suppresses epithelial-mesenchymal transition and metastasis in non-small cell lung cancer.

Publications

Silencing of RAD51AP1 suppresses epithelial-mesenchymal transition and metastasis in non-small cell lung cancer.

Similar Datasets

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