NRIP1 可调节肺腺癌细胞的增殖。

IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of biochemistry Pub Date : 2024-03-04 DOI:10.1093/jb/mvad107
Fumihiko Watanabe, Shigemitsu Sato, Takuo Hirose, Moe Endo, Akari Endo, Hiroki Ito, Koji Ohba, Takefumi Mori, Kazuhiro Takahashi
{"title":"NRIP1 可调节肺腺癌细胞的增殖。","authors":"Fumihiko Watanabe, Shigemitsu Sato, Takuo Hirose, Moe Endo, Akari Endo, Hiroki Ito, Koji Ohba, Takefumi Mori, Kazuhiro Takahashi","doi":"10.1093/jb/mvad107","DOIUrl":null,"url":null,"abstract":"<p><p>Nuclear receptor interacting protein 1 (NRIP1) is a transcription cofactor that regulates the activity of nuclear receptors and transcription factors. Functional expression of NRIP1 has been identified in multiple cancers. However, the expression and function of NRIP1 in lung adenocarcinoma have remained unclear. Thus, we aimed to clarify the NRIP1 expression and its functions in lung adenocarcinoma cells. NRIP1 and Ki-67 were immunostained in the tissue microarray section consisting of 64 lung adenocarcinoma cases, and the association of NRIP1 immunoreactivity with clinical phenotypes was examined. Survival analysis was performed in lung adenocarcinoma data from The Cancer Genome Atlas (TCGA). Human A549 lung adenocarcinoma cell line with an NRIP1-silencing technique was used in vitro study. Forty-three of 64 cases were immunostained with NRIP1. Ki-67-positive cases were more frequent in NRIP1-positive cases as opposed to NRIP1-negative cases. Higher NRIP1 mRNA expression was associated with poor prognosis in the TCGA lung adenocarcinoma data. NRIP1 was mainly located in the nucleus of A549 cells. NRIP1 silencing significantly reduced the number of living cells, suppressed cell proliferation, and induced apoptosis. These results suggest that NRIP1 participates in the progression and development of lung adenocarcinoma. Targeting NRIP1 may be a possible therapeutic strategy against lung adenocarcinoma.</p>","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"323-333"},"PeriodicalIF":2.1000,"publicationDate":"2024-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"NRIP1 regulates cell proliferation in lung adenocarcinoma cells.\",\"authors\":\"Fumihiko Watanabe, Shigemitsu Sato, Takuo Hirose, Moe Endo, Akari Endo, Hiroki Ito, Koji Ohba, Takefumi Mori, Kazuhiro Takahashi\",\"doi\":\"10.1093/jb/mvad107\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Nuclear receptor interacting protein 1 (NRIP1) is a transcription cofactor that regulates the activity of nuclear receptors and transcription factors. Functional expression of NRIP1 has been identified in multiple cancers. However, the expression and function of NRIP1 in lung adenocarcinoma have remained unclear. Thus, we aimed to clarify the NRIP1 expression and its functions in lung adenocarcinoma cells. NRIP1 and Ki-67 were immunostained in the tissue microarray section consisting of 64 lung adenocarcinoma cases, and the association of NRIP1 immunoreactivity with clinical phenotypes was examined. Survival analysis was performed in lung adenocarcinoma data from The Cancer Genome Atlas (TCGA). Human A549 lung adenocarcinoma cell line with an NRIP1-silencing technique was used in vitro study. Forty-three of 64 cases were immunostained with NRIP1. Ki-67-positive cases were more frequent in NRIP1-positive cases as opposed to NRIP1-negative cases. Higher NRIP1 mRNA expression was associated with poor prognosis in the TCGA lung adenocarcinoma data. NRIP1 was mainly located in the nucleus of A549 cells. NRIP1 silencing significantly reduced the number of living cells, suppressed cell proliferation, and induced apoptosis. These results suggest that NRIP1 participates in the progression and development of lung adenocarcinoma. Targeting NRIP1 may be a possible therapeutic strategy against lung adenocarcinoma.</p>\",\"PeriodicalId\":15234,\"journal\":{\"name\":\"Journal of biochemistry\",\"volume\":\" \",\"pages\":\"323-333\"},\"PeriodicalIF\":2.1000,\"publicationDate\":\"2024-03-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of biochemistry\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1093/jb/mvad107\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of biochemistry","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1093/jb/mvad107","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

核受体互作蛋白 1(NRIP1)是一种转录辅助因子,可调节核受体和转录因子的活性。在多种癌症中都发现了 NRIP1 的功能表达。然而,NRIP1 在肺腺癌中的表达和功能仍不清楚。因此,我们旨在明确 NRIP1 在肺腺癌细胞中的表达及其功能。我们对 64 例肺腺癌组织芯片切片中的 NRIP1 和 Ki-67 进行了免疫染色,并研究了 NRIP1 免疫反应与临床表型的关系。对癌症基因组图谱(TCGA)中的肺腺癌数据进行了生存期分析。体外研究使用了采用 NRIP1 沉默技术的人类 A549 肺腺癌细胞系。64 个病例中有 43 个被 NRIP1 免疫染色。与 NRIP1 阴性病例相比,NRIP1 阳性病例的 Ki-67 阳性率更高。在 TCGA 肺腺癌数据中,较高的 NRIP1 mRNA 表达与不良预后相关。NRIP1 主要位于 A549 细胞的细胞核中。沉默 NRIP1 能明显减少活细胞数量、抑制细胞增殖并诱导细胞凋亡。这些结果表明,NRIP1 参与了肺腺癌的进展和发展。靶向 NRIP1 可能是一种治疗肺腺癌的策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
NRIP1 regulates cell proliferation in lung adenocarcinoma cells.

Nuclear receptor interacting protein 1 (NRIP1) is a transcription cofactor that regulates the activity of nuclear receptors and transcription factors. Functional expression of NRIP1 has been identified in multiple cancers. However, the expression and function of NRIP1 in lung adenocarcinoma have remained unclear. Thus, we aimed to clarify the NRIP1 expression and its functions in lung adenocarcinoma cells. NRIP1 and Ki-67 were immunostained in the tissue microarray section consisting of 64 lung adenocarcinoma cases, and the association of NRIP1 immunoreactivity with clinical phenotypes was examined. Survival analysis was performed in lung adenocarcinoma data from The Cancer Genome Atlas (TCGA). Human A549 lung adenocarcinoma cell line with an NRIP1-silencing technique was used in vitro study. Forty-three of 64 cases were immunostained with NRIP1. Ki-67-positive cases were more frequent in NRIP1-positive cases as opposed to NRIP1-negative cases. Higher NRIP1 mRNA expression was associated with poor prognosis in the TCGA lung adenocarcinoma data. NRIP1 was mainly located in the nucleus of A549 cells. NRIP1 silencing significantly reduced the number of living cells, suppressed cell proliferation, and induced apoptosis. These results suggest that NRIP1 participates in the progression and development of lung adenocarcinoma. Targeting NRIP1 may be a possible therapeutic strategy against lung adenocarcinoma.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Journal of biochemistry
Journal of biochemistry 生物-生化与分子生物学
CiteScore
4.80
自引率
3.70%
发文量
101
审稿时长
4-8 weeks
期刊介绍: The Journal of Biochemistry founded in 1922 publishes the results of original research in the fields of Biochemistry, Molecular Biology, Cell, and Biotechnology written in English in the form of Regular Papers or Rapid Communications. A Rapid Communication is not a preliminary note, but it is, though brief, a complete and final publication. The materials described in Rapid Communications should not be included in a later paper. The Journal also publishes short reviews (JB Review) and papers solicited by the Editorial Board.
期刊最新文献
Maintenance of the Golgi Ribbon Structure by the KASH Protein Jaw1. Cellular senescence: mechanisms and relevance to cancer and aging. Bcl2l12, a novel protein interacting with Arf6, triggers Schwann cell differentiation program. Dietary methionine functions in proliferative zone maintenance and egg production via sams-1 in Caenorhabditis elegans. Variations associated with neurodevelopmental disorders affect ARF1 function and cortical development.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1