高级检索
当前位置: 首页 > 详情页

MiR-424 Promotes Non-Small Cell Lung Cancer Progression and Metastasis through Regulating the Tumor Suppressor Gene TNFAIP1

文献详情

资源类型:
WOS体系:
Pubmed体系:

收录情况: ◇ SCIE

机构: [1]Department of Radiation Oncology, The Third Affiliated Hospital of Kunming Medical University,Tumor Hospital of Yunnan Province, Kunming, [2]Department of Medical Oncology, The First AffiliatedHospital of Kunming Medical University, Kunming, [3]Department of Thoracic Surgery, The ThirdAffiliated Hospital of Kunming Medical University, Tumor Hospital of Yunnan Province, Kunming, [4]TheThird Affiliated Hospital of Kunming Medical University, Tumor Hospital of Yunnan Province, Kunming,China
出处:
ISSN:

关键词: Non-small cell lung cancer (NSCLC) miR-424 TNFAIP1 Cell migration and invasion

摘要:
Background/Aims: This study aimed to investigate the potential roles of miR-424 expression in non-small cell lung cancer (NSCLC) metastasis and growth and its underlying mechanism. Methods: The expression of miR-424 in two NSCLC cell lines (A549 and H1975) was altered by transfection with miR-424 mimic and inhibitor. Effects of miR-424 overexpression and suppression on cells migration, invasion and colony formation were analyzed. Target genes for miR-424 were predicted using bioinformatics method and then verified using luciferase assay. Effects of miR-424 expression on cell migration, invasion and proliferation were reanalyzed on the condition of TNFAIP1 was silenced. Moreover, TNFAIP1 silencing and miR-424 modified A549 cells were subcutaneous injected into node BALB/c mice to confirm the regulation of miR-424 on TNFAIP1 in regulating tumor growth. Results: Compared with the control, miR-424 overexpression significantly increased the migrated and invaded cells, as well as the proliferated colonies. TNFAIP1 was a predicted target gene for miR-424, and was negatively regulated by miR-424. TNFAIP1 silence significantly increased the migrated and invaded cells compared to that in control, while these increases were abolished by miR-424 suppression. Animal experiment further evidenced miR-424 affected tumor growth by regulating TNFAIP1. Conclusions: These data demonstrate that miR-424 may be a contributor for NSCLC progression and metastasis through involving in cell migration, invasion and proliferation via inhibiting TNFAIP1. This study may provide theoretical basis for miR-424 in NSCLC target therapeutic treatment. (C) 2017 The Author(s) Published by S. Karger AG, Basel

基金:
语种:
被引次数:
WOS:
PubmedID:
中科院(CAS)分区:
出版当年[2017]版:
大类 | 2 区 生物
小类 | 2 区 生理学 3 区 细胞生物学
最新[2023]版:
JCR分区:
出版当年[2016]版:
Q1 PHYSIOLOGY Q2 CELL BIOLOGY
最新[2023]版:
Q2 PHYSIOLOGY Q3 CELL BIOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2016版] 出版当年五年平均 出版前一年[2015版] 出版后一年[2017版]

第一作者:
第一作者机构: [1]Department of Radiation Oncology, The Third Affiliated Hospital of Kunming Medical University,Tumor Hospital of Yunnan Province, Kunming,
共同第一作者:
通讯作者:
通讯机构: [1]Department of Radiation Oncology, The Third Affiliated Hospital of Kunming Medical University,Tumor Hospital of Yunnan Province, Kunming, [*1]Department of Radiation Oncology, The Third Affiliated Hospital of Kunming Medical University, Tumor Hospital of Yunnan Province, No.519, Kunzhou Road, Kunming 650018, (China)
推荐引用方式(GB/T 7714):
APA:
MLA:

资源点击量:82490 今日访问量:0 总访问量:681 更新日期:2025-01-01 建议使用谷歌、火狐浏览器 常见问题

版权所有©2020 云南省第一人民医院 技术支持:重庆聚合科技有限公司 地址:云南省昆明市西山区金碧路157号