[Villin-like protein VILL suppresses proliferation of nasopharyngeal carcinoma cells by interacting with LMO7 protein].

Q3 Medicine
Yumei Zeng, Jike Li, Zhongxi Huang, Yibo Zhou
{"title":"[Villin-like protein VILL suppresses proliferation of nasopharyngeal carcinoma cells by interacting with LMO7 protein].","authors":"Yumei Zeng, Jike Li, Zhongxi Huang, Yibo Zhou","doi":"10.12122/j.issn.1673-4254.2025.05.07","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>To elucidate the molecular mechanism by which villin-like protein VILL (VILL) inhibits proliferation of nasopharyngeal carcinoma (NPC) cells.</p><p><strong>Methods: </strong>Co-immunoprecipitation (CO-IP) assay, mass spectrometry, Western blotting, immunofluorescence staining, and GST pull-down assay were employed to identify and confirm the protein interacting with VILL that had the highest abundance in NPC cell lines. Transgenic experiments were conducted in both NPC cell lines and nude mice to validate the regulatory role of VILL and its target protein in NPC proliferation. Immunohistochemistry was utilized to assess the correlation of the expression levels of VILL and its target protein in clinical tissue specimens of NPC with the clinical features of the patients.</p><p><strong>Results: </strong>In NPC cell lines (HONE1 EBV and S18), VILL was found to interact most abundantly with the E3 ubiquitin ligase LMO7, and both proteins co-localized in the cytoplasm with direct interactions. Overexpression of LMO7 partially counteracted the inhibitory effect of VILL on NPC cell proliferation. The expression of VILL was significantly downregulated in 136 NPC tissue samples compared to 67 non-cancerous nasopharyngeal tissues (<i>P</i><0.00001) with close correlation with clinical T stage (<i>P</i>=0.04), N stage (<i>P</i>=0.01), and M stage (<i>P</i>=0.013), whereas LMO7 was highly expressed in all the NPC tissues.</p><p><strong>Conclusions: </strong>VILL overexpression inhibits NPC proliferation probably by suppressing the oncogenic function of LMO7.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 5","pages":"954-961"},"PeriodicalIF":0.0000,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12104744/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"南方医科大学学报杂志","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.12122/j.issn.1673-4254.2025.05.07","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0

Abstract

Objectives: To elucidate the molecular mechanism by which villin-like protein VILL (VILL) inhibits proliferation of nasopharyngeal carcinoma (NPC) cells.

Methods: Co-immunoprecipitation (CO-IP) assay, mass spectrometry, Western blotting, immunofluorescence staining, and GST pull-down assay were employed to identify and confirm the protein interacting with VILL that had the highest abundance in NPC cell lines. Transgenic experiments were conducted in both NPC cell lines and nude mice to validate the regulatory role of VILL and its target protein in NPC proliferation. Immunohistochemistry was utilized to assess the correlation of the expression levels of VILL and its target protein in clinical tissue specimens of NPC with the clinical features of the patients.

Results: In NPC cell lines (HONE1 EBV and S18), VILL was found to interact most abundantly with the E3 ubiquitin ligase LMO7, and both proteins co-localized in the cytoplasm with direct interactions. Overexpression of LMO7 partially counteracted the inhibitory effect of VILL on NPC cell proliferation. The expression of VILL was significantly downregulated in 136 NPC tissue samples compared to 67 non-cancerous nasopharyngeal tissues (P<0.00001) with close correlation with clinical T stage (P=0.04), N stage (P=0.01), and M stage (P=0.013), whereas LMO7 was highly expressed in all the NPC tissues.

Conclusions: VILL overexpression inhibits NPC proliferation probably by suppressing the oncogenic function of LMO7.

[绒毛样蛋白VILL通过与LMO7蛋白相互作用抑制鼻咽癌细胞增殖]。
目的:探讨绒毛蛋白样蛋白(vilin -like protein, VILL)抑制鼻咽癌细胞增殖的分子机制。方法:采用共免疫沉淀(CO-IP)法、质谱法、免疫印迹法、免疫荧光染色法、GST下拉法等方法,鉴定鼻咽癌细胞株中丰度最高的与VILL相互作用的蛋白。在鼻咽癌细胞系和裸鼠中进行转基因实验,验证了VILL及其靶蛋白在鼻咽癌细胞增殖中的调控作用。应用免疫组织化学方法评估鼻咽癌临床组织标本中VILL及其靶蛋白的表达水平与患者临床特征的相关性。结果:在鼻咽癌细胞系(HONE1 EBV和S18)中,发现VILL与E3泛素连接酶LMO7的相互作用最为丰富,并且两种蛋白在细胞质中共定位并直接相互作用。LMO7过表达部分抵消了VILL对鼻咽癌细胞增殖的抑制作用。与67例非癌性鼻咽癌组织(PP=0.04)、N期(P=0.01)和M期(P=0.013)相比,136例鼻咽癌组织中VILL的表达显著下调,而LMO7在所有鼻咽癌组织中均高表达。结论:VILL过表达可能通过抑制LMO7的致癌功能来抑制鼻咽癌的增殖。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
南方医科大学学报杂志
南方医科大学学报杂志 Medicine-Medicine (all)
CiteScore
1.50
自引率
0.00%
发文量
208
期刊介绍:
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信