骨硅蛋白通过抑制 miR-150-5p 的表达促进肺癌的抗肿瘤能力

IF 5.3
Le Huynh Hoai Thuong, Chang-Lun Huang, Yi-Chin Fong, Chun-Lin Liu, Jeng-Hung Guo, Chih-Ying Wu, Po-I Liu, Chih-Hsin Tang
{"title":"骨硅蛋白通过抑制 miR-150-5p 的表达促进肺癌的抗肿瘤能力","authors":"Le Huynh Hoai Thuong,&nbsp;Chang-Lun Huang,&nbsp;Yi-Chin Fong,&nbsp;Chun-Lin Liu,&nbsp;Jeng-Hung Guo,&nbsp;Chih-Ying Wu,&nbsp;Po-I Liu,&nbsp;Chih-Hsin Tang","doi":"10.1111/jcmm.70155","DOIUrl":null,"url":null,"abstract":"<p>Metastatic lung cancer is a highly prevalent cancer with a very low chance of long-term survival. Metastasis at secondary sites requires that cancer cells develop anoikis resistance to survive during circulation. High levels of bone sialoprotein (BSP), a member of the small integrin-binding ligand N-linked glycoproteins (SIBLINGs), have been shown to promote the spread of lung cancer cells; however, the effects of BSP in anoikis resistance are largely unknown. In this study, we determined that BSP promotes anoikis resistance in lung cancer cells. BSP was also shown to promote the expression of E-cadherin and vimentin (epithelial-to-mesenchymal transition markers, which have been utilized as indicators of anoikis resistance). It appears that BSP facilitates MMP-14-dependent anoikis resistance by inhibiting the synthesis of miR-150-5p and activating the ERK signalling pathway. Knockdown of BSP expression was shown to block lung cancer metastasis by lowering anoikis resistance <i>in vivo</i>. These results indicate that BSP is a promising target to deal with anoikis resistance and metastasis in human lung cancers.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 20","pages":""},"PeriodicalIF":5.3000,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70155","citationCount":"0","resultStr":"{\"title\":\"Bone sialoprotein facilitates anoikis resistance in lung cancer by inhibiting miR-150-5p expression\",\"authors\":\"Le Huynh Hoai Thuong,&nbsp;Chang-Lun Huang,&nbsp;Yi-Chin Fong,&nbsp;Chun-Lin Liu,&nbsp;Jeng-Hung Guo,&nbsp;Chih-Ying Wu,&nbsp;Po-I Liu,&nbsp;Chih-Hsin Tang\",\"doi\":\"10.1111/jcmm.70155\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>Metastatic lung cancer is a highly prevalent cancer with a very low chance of long-term survival. Metastasis at secondary sites requires that cancer cells develop anoikis resistance to survive during circulation. High levels of bone sialoprotein (BSP), a member of the small integrin-binding ligand N-linked glycoproteins (SIBLINGs), have been shown to promote the spread of lung cancer cells; however, the effects of BSP in anoikis resistance are largely unknown. In this study, we determined that BSP promotes anoikis resistance in lung cancer cells. BSP was also shown to promote the expression of E-cadherin and vimentin (epithelial-to-mesenchymal transition markers, which have been utilized as indicators of anoikis resistance). It appears that BSP facilitates MMP-14-dependent anoikis resistance by inhibiting the synthesis of miR-150-5p and activating the ERK signalling pathway. Knockdown of BSP expression was shown to block lung cancer metastasis by lowering anoikis resistance <i>in vivo</i>. These results indicate that BSP is a promising target to deal with anoikis resistance and metastasis in human lung cancers.</p>\",\"PeriodicalId\":101321,\"journal\":{\"name\":\"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE\",\"volume\":\"28 20\",\"pages\":\"\"},\"PeriodicalIF\":5.3000,\"publicationDate\":\"2024-10-28\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70155\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/jcmm.70155\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/jcmm.70155","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

转移性肺癌是一种高发癌症,长期存活的几率非常低。继发部位的转移需要癌细胞在循环过程中发展出抗免疫力才能存活。高水平的骨硅蛋白(BSP)是小整合素结合配体N-连接糖蛋白(SIBLINGs)的成员之一,已被证明能促进肺癌细胞的扩散;然而,BSP在抗免疫反应中的作用在很大程度上是未知的。在这项研究中,我们确定 BSP 能促进肺癌细胞的耐药力。研究还表明,BSP 还能促进 E-cadherin 和 vimentin(上皮细胞向间质转化的标志物,已被用作抗 anoikis 的指标)的表达。由此看来,BSP 通过抑制 miR-150-5p 的合成和激活 ERK 信号通路,促进了 MMP-14 依赖性厌氧菌抗性。研究表明,在体内敲除 BSP 的表达可通过降低耐 anoikis 性来阻止肺癌转移。这些结果表明,BSP 是解决人类肺癌耐 anoikis 性和转移问题的一个有前途的靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Bone sialoprotein facilitates anoikis resistance in lung cancer by inhibiting miR-150-5p expression

Bone sialoprotein facilitates anoikis resistance in lung cancer by inhibiting miR-150-5p expression

Metastatic lung cancer is a highly prevalent cancer with a very low chance of long-term survival. Metastasis at secondary sites requires that cancer cells develop anoikis resistance to survive during circulation. High levels of bone sialoprotein (BSP), a member of the small integrin-binding ligand N-linked glycoproteins (SIBLINGs), have been shown to promote the spread of lung cancer cells; however, the effects of BSP in anoikis resistance are largely unknown. In this study, we determined that BSP promotes anoikis resistance in lung cancer cells. BSP was also shown to promote the expression of E-cadherin and vimentin (epithelial-to-mesenchymal transition markers, which have been utilized as indicators of anoikis resistance). It appears that BSP facilitates MMP-14-dependent anoikis resistance by inhibiting the synthesis of miR-150-5p and activating the ERK signalling pathway. Knockdown of BSP expression was shown to block lung cancer metastasis by lowering anoikis resistance in vivo. These results indicate that BSP is a promising target to deal with anoikis resistance and metastasis in human lung cancers.

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
CiteScore
11.50
自引率
0.00%
发文量
0
期刊介绍: The Journal of Cellular and Molecular Medicine serves as a bridge between physiology and cellular medicine, as well as molecular biology and molecular therapeutics. With a 20-year history, the journal adopts an interdisciplinary approach to showcase innovative discoveries. It publishes research aimed at advancing the collective understanding of the cellular and molecular mechanisms underlying diseases. The journal emphasizes translational studies that translate this knowledge into therapeutic strategies. Being fully open access, the journal is accessible to all readers.
×
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