PUM2通过抑制BTG1表达促进胶质母细胞瘤细胞增殖和迁移。

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2019-01-01 DOI:10.1247/csf.18030
Yuanyu Wang, Weili Sun, Jiankai Yang, Liang Yang, Chen Li, Hongjiang Liu, Xiaopeng Liu, Baohua Jiao
{"title":"PUM2通过抑制BTG1表达促进胶质母细胞瘤细胞增殖和迁移。","authors":"Yuanyu Wang,&nbsp;Weili Sun,&nbsp;Jiankai Yang,&nbsp;Liang Yang,&nbsp;Chen Li,&nbsp;Hongjiang Liu,&nbsp;Xiaopeng Liu,&nbsp;Baohua Jiao","doi":"10.1247/csf.18030","DOIUrl":null,"url":null,"abstract":"<p><p>PUM2, an RNA binding protein, is known to promote stem cell proliferation via repressing expressions of cell cycle genes. Similar with stem cells, malignant cells are characterized by unlimited proliferation and remote migration. However, roles of PUM2 in cancer development are controversial. Here, we investigated PUM2's role in glioblastoma development and its relationship with the cell cycle regulator BTG1. Immunoblotting and RT-qPCR were used to evaluate protein expression level and transcript level, respectively. ShRNAs were designed to knock down PUM2 and BTG1 expression. CCK-8 assay was used to evaluate cell viability. Cell migration assay and evasion assay were used to evaluate metastatic capability of glioblastoma cell. RNA pull-down assay and RNA immunoprecipitation assay were used to test the interaction between PUM2 and BTG1 3'UTR. PUM2 expression is elevated in glioblastoma tumor tissues as well as glioblastoma cell lines. PUM2 knockdown remarkably suppresses glioblastoma cell proliferation and migration. In addition, PUM2 knockdown increases BTG1 expression. RNA pull-down assay and RNA immunoprecipitation assay show PUM2 binds to BTG1 3'UTR directly. Furthermore, knockdown of BTG1 reverses the effect of PUM2 knockdown on glioblastoma cell proliferation and migration. Our results suggest that PUM2 promote glioblastoma development via repressing BTG1 expression.Key words: PUM2, BTG1, glioblastoma, cell proliferation, metastasis.</p>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1247/csf.18030","citationCount":"15","resultStr":"{\"title\":\"PUM2 Promotes Glioblastoma Cell Proliferation and Migration via Repressing BTG1 Expression.\",\"authors\":\"Yuanyu Wang,&nbsp;Weili Sun,&nbsp;Jiankai Yang,&nbsp;Liang Yang,&nbsp;Chen Li,&nbsp;Hongjiang Liu,&nbsp;Xiaopeng Liu,&nbsp;Baohua Jiao\",\"doi\":\"10.1247/csf.18030\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>PUM2, an RNA binding protein, is known to promote stem cell proliferation via repressing expressions of cell cycle genes. Similar with stem cells, malignant cells are characterized by unlimited proliferation and remote migration. However, roles of PUM2 in cancer development are controversial. Here, we investigated PUM2's role in glioblastoma development and its relationship with the cell cycle regulator BTG1. Immunoblotting and RT-qPCR were used to evaluate protein expression level and transcript level, respectively. ShRNAs were designed to knock down PUM2 and BTG1 expression. CCK-8 assay was used to evaluate cell viability. Cell migration assay and evasion assay were used to evaluate metastatic capability of glioblastoma cell. RNA pull-down assay and RNA immunoprecipitation assay were used to test the interaction between PUM2 and BTG1 3'UTR. PUM2 expression is elevated in glioblastoma tumor tissues as well as glioblastoma cell lines. PUM2 knockdown remarkably suppresses glioblastoma cell proliferation and migration. In addition, PUM2 knockdown increases BTG1 expression. RNA pull-down assay and RNA immunoprecipitation assay show PUM2 binds to BTG1 3'UTR directly. Furthermore, knockdown of BTG1 reverses the effect of PUM2 knockdown on glioblastoma cell proliferation and migration. Our results suggest that PUM2 promote glioblastoma development via repressing BTG1 expression.Key words: PUM2, BTG1, glioblastoma, cell proliferation, metastasis.</p>\",\"PeriodicalId\":2,\"journal\":{\"name\":\"ACS Applied Bio Materials\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":4.6000,\"publicationDate\":\"2019-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1247/csf.18030\",\"citationCount\":\"15\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"ACS Applied Bio Materials\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1247/csf.18030\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"MATERIALS SCIENCE, BIOMATERIALS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1247/csf.18030","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
引用次数: 15

摘要

PUM2是一种RNA结合蛋白,已知通过抑制细胞周期基因的表达来促进干细胞增殖。与干细胞相似,恶性细胞具有无限增殖和远程迁移的特点。然而,PUM2在癌症发展中的作用仍存在争议。在这里,我们研究了PUM2在胶质母细胞瘤发育中的作用及其与细胞周期调节因子BTG1的关系。采用免疫印迹法和RT-qPCR法分别检测蛋白表达水平和转录物水平。shrna被设计用于敲低PUM2和BTG1的表达。CCK-8法测定细胞活力。采用细胞迁移法和逃避法评价胶质母细胞瘤细胞的转移能力。采用RNA拉下法和RNA免疫沉淀法检测PUM2与BTG1 3'UTR的相互作用。PUM2在胶质母细胞瘤肿瘤组织和胶质母细胞瘤细胞系中表达升高。PUM2敲低显著抑制胶质母细胞瘤细胞的增殖和迁移。此外,PUM2敲低会增加BTG1的表达。RNA拉下实验和RNA免疫沉淀实验显示PUM2直接结合BTG1 3'UTR。此外,BTG1的敲低逆转了PUM2敲低对胶质母细胞瘤细胞增殖和迁移的影响。我们的研究结果表明PUM2通过抑制BTG1的表达促进胶质母细胞瘤的发展。关键词:PUM2, BTG1,胶质母细胞瘤,细胞增殖,转移
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
PUM2 Promotes Glioblastoma Cell Proliferation and Migration via Repressing BTG1 Expression.

PUM2, an RNA binding protein, is known to promote stem cell proliferation via repressing expressions of cell cycle genes. Similar with stem cells, malignant cells are characterized by unlimited proliferation and remote migration. However, roles of PUM2 in cancer development are controversial. Here, we investigated PUM2's role in glioblastoma development and its relationship with the cell cycle regulator BTG1. Immunoblotting and RT-qPCR were used to evaluate protein expression level and transcript level, respectively. ShRNAs were designed to knock down PUM2 and BTG1 expression. CCK-8 assay was used to evaluate cell viability. Cell migration assay and evasion assay were used to evaluate metastatic capability of glioblastoma cell. RNA pull-down assay and RNA immunoprecipitation assay were used to test the interaction between PUM2 and BTG1 3'UTR. PUM2 expression is elevated in glioblastoma tumor tissues as well as glioblastoma cell lines. PUM2 knockdown remarkably suppresses glioblastoma cell proliferation and migration. In addition, PUM2 knockdown increases BTG1 expression. RNA pull-down assay and RNA immunoprecipitation assay show PUM2 binds to BTG1 3'UTR directly. Furthermore, knockdown of BTG1 reverses the effect of PUM2 knockdown on glioblastoma cell proliferation and migration. Our results suggest that PUM2 promote glioblastoma development via repressing BTG1 expression.Key words: PUM2, BTG1, glioblastoma, cell proliferation, metastasis.

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
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
期刊最新文献
A Systematic Review of Sleep Disturbance in Idiopathic Intracranial Hypertension. Advancing Patient Education in Idiopathic Intracranial Hypertension: The Promise of Large Language Models. Anti-Myelin-Associated Glycoprotein Neuropathy: Recent Developments. Approach to Managing the Initial Presentation of Multiple Sclerosis: A Worldwide Practice Survey. Association Between LACE+ Index Risk Category and 90-Day Mortality After Stroke.
×
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