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Overexpression of miR-30a in lung adenocarcinoma A549 cell line inhibits migration and invasion via targeting EYA2
  • ISSN号:1672-9145
  • 期刊名称:《生物化学与生物物理学报:英文版》
  • 时间:0
  • 分类:Q25[生物学—细胞生物学] Q753[生物学—分子生物学]
  • 作者机构:[1]School of Medicine, Yunnan University, Kunming 650091, China, [2]Department of Thoracic Surgery,Third Affiliated Hospital of Kunming Medical University, Kunming 650118, China
  • 相关基金:the grants from the National Natural Science Foundation of China (Nos. 81372360 and 81460435) and the Key Projects of Applied Basic Research of Yunnan Province (No. 2014FA022).
中文摘要:

MicroRNAs (miRNAs ) 是与癌症的致病有关的小非编码的 RNA 并且仔细的一个班。增加的证据显示 miR-30a 在癌症的发展期间起一个深刻作用。然而,在 non-small-cell 肺癌症(NSCLC ) 的 miR-30a 的功能仍然是模糊的。这里,我们发现 miR-30a 被 qRT-PCR 从 14 个病人在肺腺癌 A549 房间并且在织物样品减少,并且也发现在 A549 房间的 miR-30a 的 overexpression 由愈合创伤的试金禁止了移植和侵略然而并非房间增长和房间周期前进, matrigel 侵略试金,基于山的房间增长试金,和流动 基于cytometry 的房间周期分析分别地。我们进一步在肺腺癌房间行探索了 miR-30a-mediated 基因规定的潜在的机制。EYA2 是 miR-30a 的一个预言的目标,并且 EYA2 表示被 miR-30a 在乳癌房间禁止,这被发现了。我们证明 EYA2 是由在 A549 房间使用双酶的记者试金的 miR-30a 的一个直接目标并且证明 EYA2 蛋白质层次相反地在 A549 和 BEAS-2B 房间与 miR-30a 表示被相关。另外,我们也与表示向量和 miR-30a 模仿的 EYA2 由 cotransfection 在 A549 房间证实了 EYA2 overexpression 的营救效果。一起拿,我们的结果证明在肺腺癌 A549 房间的 miR-30a 的 overexpression 能禁止房间移植和侵略,它部分被归因于 EYA2 的减少表示。我们的调查结果建议 miR-30a 以后可以为肺腺癌的治疗被用作一个新潜在的目标。

英文摘要:

Mic:roRNAs (miRNAs) are a class of small non-coding RNAs and closely related to the pathogenesis of cancers. Increasing evidence indicates that miR-30a plays a profound role during the development of cancers. However, the functions of miR-30a in non-small-cell lung cancer (NSCLC) are still ambigu- ous. Here we found that miR-30a was decreased in lung adenocarcinoma A549 cells and in tissue samples from 14 patients by qRT-PCR, and also found that overexpression of miR-30a in A549 cells inhibited migration and invasion but not cell proliferation and: cell cycle progression by wound-healing assay, matrigel invasion assay, MTS-based cell proliferation assay, and flow cytome- try-based cell cycle analysis, respectively. We further explored the potential mechanism of miR-3Oa- mediated gene regulation in lung adenocarcinoma cell lines. EYA2 is a predicted target of miR-30a, and it has been found that EYA2expression is inhibited by miR-30a in breast cancer cells. We demon- strated that EYA2 is a direct target of miR-30a by using the dual-luciferase reporter assay in A549 cells and showed that EYA2 protein levels are inversely correlated with miR-30a expression in A549 and BEAS-2B cells. In addition, we also confirmed the rescue effects of EYA2overexpression in A549 cells by cotransfection with EYA2 expression vector and miR-30a mimics, Taken together, our results demonstrate that overexpression of miR-30a in lung adenocarcinoma A549 cells can inhibit cell mi- gration and invasion, which is partially attributed to the decrease of EYA2 expression. Our findings suggest that miR-30a may be used as a new potential target for the treatment of lung adenocarcinoma in the future.

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期刊信息
  • 《生物化学与生物物理学报:英文版》
  • 北大核心期刊(2004版)
  • 主管单位:
  • 主办单位:中国科学院上海生物化学研究所
  • 主编:
  • 地址:上海岳阳路319号
  • 邮编:200031
  • 邮箱:abbs@sibs.ac.cn
  • 电话:021-54920956 54920955
  • 国际标准刊号:ISSN:1672-9145
  • 国内统一刊号:ISSN:31-1940/Q
  • 邮发代号:4-210
  • 获奖情况:
  • 国内外数据库收录:
  • 美国化学文摘(网络版),英国农业与生物科学研究中心文摘,荷兰文摘与引文数据库,美国生物医学检索系统,美国剑桥科学文摘,美国科学引文索引(扩展库),美国生物科学数据库,英国动物学记录,日本日本科学技术振兴机构数据库,中国中国科技核心期刊,中国北大核心期刊(2004版),英国英国皇家化学学会文摘,中国北大核心期刊(2000版)
  • 被引量:5851