PRMT7 contributes to the metastasis phenotype in human non-small-cell lung cancer cells possibly through the interaction with HSPA5 and EEF2

doi:10.2147/OTT.S166412

科研成果详情

题名	PRMT7 contributes to the metastasis phenotype in human non-small-cell lung cancer cells possibly through the interaction with HSPA5 and EEF2
作者	Cheng, Dezhi1,2; He, Zhifeng2; Zheng, Liangcheng2; Xie, Deyao2; Dong, Shangwen 1; Zhang, Peng 1
发表日期	2018-12-31
发表期刊	ONCOTARGETS AND THERAPY 影响因子和分区
语种	英语
原始文献类型	Article
关键词	human non-small-cell lung cancer arginine methylation PRMT7 protein-protein interaction HSPA5 EEF2
其他关键词	PROTEIN ARGININE METHYLTRANSFERASES ; GENE ; INVASION ; TRANSITION
摘要	Background: Non-small-cell lung cancer (NSCLC) constitutes the leading cause of cancer death in humans. Previous studies revealed the essential role of the protein arginine methyltransferase 7 (PRMT7) in promoting metastasis in breast cancer. However, its function and potential mechanism in NSCLC remain unclear. Materials and methods: The gene expression of PRMT7 between lung cancer tissues and normal tissues was studied with online database (http://medicalgenome.kribb.re.kr/ GENT/). NSCLC cell lines with specific gene overexpression were constructed with lentivims transduction. Matrigel invasion and colony formation assays were performed to evaluate the invasion and colony formation abilities. Co-immunoprecipitation coupled with mass spectrometry analysis was performed to explore the potential interaction proteins of PRMT7. Bioinformatic analysis was performed with Gene Ontology and Kyoto Encyclopedia of Genes and Genomes databases. Results: Online analysis of gene expression patterns revealed the relatively high expression of PRMT7 in lung cancer tissues. PRMT7 overexpression was able to promote the invasion and colony formation of A549 and SPC-A1 cells. A total of 19 in-common proteins shared by both NSCLC cell lines were identified to be interacting with PRMT7 and found to participate in a wide variety of pathways and protein-protein interactions according to bioinformatic analysis. Among them, HSPA5 and EEF2 were further investigated for their essential roles in PRMT7-promoted NSCLC cell invasion. Conclusion: Our results suggested PRMT7 overexpression was able to promote metastasis in NSCLC possibly through the interaction with HSPA5 and EEF2, which provides the potential mechanism of oncogenesis in lung cancer.
资助项目	Natural Science Foundation of Zhejiang ProvinceNatural Science Foundation of Zhejiang Province [LY14H160042]; Wenzhou public welfare science and technology plan [Y20160047, Y20160049]
出版者	DOVE MEDICAL PRESS LTD
出版地	ALBANY
ISSN	1178-6930
卷号	11 页码:4869-4876
DOI	10.2147/OTT.S166412
页数	8
WOS类目	Biotechnology & Applied Microbiology ; Oncology
WOS研究方向	Biotechnology & Applied Microbiology ; Oncology
WOS记录号	WOS:000441753100005
收录类别	SCIE ; PUBMED ; SCOPUS
URL	查看原文
PubMed ID	30147338
PMC记录号	PMC6098420
SCOPUSEID	2-s2.0-85058678217
通讯作者地址	[Zhang, Peng]Department of Thoracic Surgery,Tianjin Medical University General Hospital,154 Anshan Road, Heping District,Tianjin City,China
Scopus学科分类	Oncology;Pharmacology (medical)
引用统计	被引频次：19[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/18579
专题	附属第一医院_心血管内科
通讯作者	Zhang, Peng
作者单位	1.Department of Thoracic Surgery,Tianjin Medical University General Hospital,Tianjin,China; 2.Department of Thoracic Cardiovascular,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,China
第一作者单位	附属第一医院; 第一临床医学院（信息与工程学院）、附属第一医院
推荐引用方式 GB/T 7714	Cheng, Dezhi,He, Zhifeng,Zheng, Liangcheng,et al. PRMT7 contributes to the metastasis phenotype in human non-small-cell lung cancer cells possibly through the interaction with HSPA5 and EEF2[J]. ONCOTARGETS AND THERAPY,2018,11:4869-4876.
APA	Cheng, Dezhi, He, Zhifeng, Zheng, Liangcheng, Xie, Deyao, Dong, Shangwen, & Zhang, Peng. (2018). PRMT7 contributes to the metastasis phenotype in human non-small-cell lung cancer cells possibly through the interaction with HSPA5 and EEF2. ONCOTARGETS AND THERAPY, 11, 4869-4876.
MLA	Cheng, Dezhi,et al."PRMT7 contributes to the metastasis phenotype in human non-small-cell lung cancer cells possibly through the interaction with HSPA5 and EEF2".ONCOTARGETS AND THERAPY 11(2018):4869-4876.