题名 | Identification of curcumin-inhibited extracellular matrix receptors in non-small cell lung cancer A549 cells by RNA sequencing |
作者 | |
发表日期 | 2017-06-15 |
发表期刊 | TUMOR BIOLOGY 影响因子和分区 |
语种 | 英语 |
原始文献类型 | Article |
关键词 | Curcumin RNA sequencing lung cancer cell migration extracellular matrix receptors |
其他关键词 | FOCAL ADHESION KINASE ; PI3K/AKT SIGNALING PATHWAY ; DOWN-REGULATION ; EXPRESSION ; SURVIVAL ; APOPTOSIS ; INVASION ; RESISTANCE ; MIGRATION ; PROLIFERATION |
摘要 | Curcumin is a potent anti-cancer drug in several types of human cancers. Despite of several preclinical and clinical studies of curcumin, the precise mechanism of curcumin in cancer prevention has remained unclear. In our study, we for the first time investigated whole transcriptome alteration in A549 non-small cell lung cancer (NSCLC) cell lines after treatment with curcumin using RNA sequencing. We found that lots of genes and signaling pathways were significantly altered after curcumin treatment in A549 cells. With bioinformatics approaches (gene ontology, Kyoto Encyclopedia of Genes and Genomes, and STRING), we found that those curcumin altered genes were not only the genes that induce cell death but also those extracellular matrix receptors and mitogen-activated protein kinase signaling pathway genes which regulate cell migration and proliferation. Among those significantly altered genes, eight genes (COL1A1, COL4A1, COL5A1, LAMA5, ITGA3, ITGA2B, DDIT3, and DUSP1) were further examined by quantitative reverse transcription polymerase chain reaction and western blot analysis in four non-small cell lung cancer cell lines. Both in cell lines and in mouse model, the extracellular matrix receptors including the integrin (ITGA3 and ITGA2B), collagen (COL5A1), and laminin (LAMA5) were significantly inhibited by curcumin at messenger RNA and protein levels. Functional studies confirmed that curcumin not only induced A549 cell death but also repressed cell proliferation and migration by regulating extracellular matrix receptors. Collectively, our study suggests that curcumin may be used as a promising drug candidate for intervening lung cancer in future studies. |
资助项目 | Natural Science Foundation of Zhejiang ProvinceNatural Science Foundation of Zhejiang Province [LZ15H220001, LY14H160005]; Zhejiang medical and Health Ministry Training Program [2015PYA009]; National Natural Science Foundation of China (CN)National Natural Science Foundation of China (NSFC) [81402529] |
出版者 | SAGE PUBLICATIONS LTD |
出版地 | LONDON |
ISSN | 1010-4283 |
EISSN | 1423-0380 |
卷号 | 39期号:6 |
DOI | 10.1177/1010428317705334 |
页数 | 13 |
WOS类目 | Oncology |
WOS研究方向 | Oncology |
WOS记录号 | WOS:000403618600001 |
收录类别 | SCIE ; SCOPUS ; PUBMED |
URL | 查看原文 |
PubMed ID | 28618934 |
SCOPUSEID | 2-s2.0-85025112495 |
通讯作者地址 | [Yang, Shuan-Ying]Department of Respiratory Medicine,The Second Affiliated Hospital of Xi’an Jiaotong University,Xi’an,710004,China |
Scopus学科分类 | Cancer Research |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | https://kms.wmu.edu.cn/handle/3ETUA0LF/6183 |
专题 | 第一临床医学院(信息与工程学院)、附属第一医院_急诊医学 附属第一医院 |
通讯作者 | Yang, Shuan-Ying |
作者单位 | 1.Department of Respiratory Medicine,The Second Affiliated Hospital of Xi’an Jiaotong University,Xi’an,China; 2.Department of Emergency Medicine,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,China; 3.Cancer Research Institute,Hangzhou Cancer Hospital,Hangzhou,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; 急诊医学 |
推荐引用方式 GB/T 7714 | Li, Huiping,Wu, Hongjin,Zhang, Hongfang,et al. Identification of curcumin-inhibited extracellular matrix receptors in non-small cell lung cancer A549 cells by RNA sequencing[J]. TUMOR BIOLOGY,2017,39(6). |
APA | Li, Huiping., Wu, Hongjin., Zhang, Hongfang., Li, Ying., Li, Shuang., ... & Yang, Shuan-Ying. (2017). Identification of curcumin-inhibited extracellular matrix receptors in non-small cell lung cancer A549 cells by RNA sequencing. TUMOR BIOLOGY, 39(6). |
MLA | Li, Huiping,et al."Identification of curcumin-inhibited extracellular matrix receptors in non-small cell lung cancer A549 cells by RNA sequencing".TUMOR BIOLOGY 39.6(2017). |
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