• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

GLIPR1调节胶质瘤细胞中的TIMP1-CD63-ITGB1-AKT信号通路，并诱导星形胶质瘤发生恶性转化。

GLIPR1 regulates the TIMP1-CD63-ITGB1-AKT signaling pathway in glioma cells and induces malignant transformation of astroglioma.

作者信息

Li Feng, Zhang Weifeng, Wang Ming, Jia Pifeng

机构信息

Department of Neurosurgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

出版信息

Transl Cancer Res. 2022 Jul;11(7):2205-2216. doi: 10.21037/tcr-21-2413.

DOI:10.21037/tcr-21-2413
PMID:35966296
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9372201/
Abstract

BACKGROUND

Astrocytoma (ACM) is characterized by high recurrence rate, high mortality, and extremely poor clinical prognosis. The new diagnostic and prognostic tumor markers related to ACM was found to improve the diagnosis rate and reduce the poor prognosis.

METHODS

The activity of SHC-44 and SW1783 cells under the regulation of glioma pathogenesis-related protein 1 (GLIPR1) was investigated by CCK8 analysis. The effect of GLIPR1 on the proliferation of SHC-44 and SW1783 cells was analyzed by cell colony-forming experiment. The migration of SHC-44 and SW1783 cells under the regulation of GLIPR1 was analyzed by transwell assay. The effects of GLIPR1 on the invasion and migration of SHC-44 and SW1783 cells were analyzed by cell scratch test and transwell assay. Immunofluorescence and Co-IP assays were employed to analyze the expression characteristics of GLIPR1 and CD63 proteins. The effect of GLIPR1 on the protein expression of GLIPR1, TIMP1, CD63, ITGB1, and AKT in SHC-44 and SW1783 cells was analyzed by western blot. The effect of anti-AKT on the protein expression of GLIPR1, TIMP1, CD63, ITGB1, and AKT in SHC-44 and SW1783 cells was performed by western blot.

RESULTS

The outcomes revealed that GLIPR1 could enhance the activity, proliferation, migration, and invasion of ACM cells, which might be associated with the activation of the TIMP1-CD63-ITGB1-AKT signaling pathway.

CONCLUSIONS

Taken together, GLIPR1 might be a potential target for the prevention or management of ACM in the clinic.

摘要

背景

星形细胞瘤（ACM）具有高复发率、高死亡率和极差的临床预后等特征。发现与ACM相关的新型诊断和预后肿瘤标志物可提高诊断率并改善不良预后。

方法

通过CCK8分析研究神经胶质瘤发病相关蛋白1（GLIPR1）调控下SHC - 44和SW1783细胞的活性。通过细胞集落形成实验分析GLIPR1对SHC - 44和SW1783细胞增殖的影响。通过Transwell实验分析GLIPR1调控下SHC - 44和SW1783细胞的迁移情况。通过细胞划痕实验和Transwell实验分析GLIPR1对SHC - 44和SW1783细胞侵袭和迁移的影响。采用免疫荧光和免疫共沉淀实验分析GLIPR1和CD63蛋白的表达特征。通过蛋白质印迹法分析GLIPR1对SHC - 44和SW1783细胞中GLIPR1、TIMP1、CD63、ITGB1和AKT蛋白表达的影响。通过蛋白质印迹法检测抗AKT对SHC - 44和SW1783细胞中GLIPR1、TIMP1、CD63、ITGB1和AKT蛋白表达的作用。

结果

结果显示，GLIPR1可增强ACM细胞的活性、增殖、迁移和侵袭能力，这可能与TIMP1 - CD63 - ITGB1 - AKT信号通路的激活有关。

结论

综上所述，GLIPR1可能是临床上预防或治疗ACM的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/ed3dcb8ca936/tcr-11-07-2205-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/31898e689fbf/tcr-11-07-2205-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/861fb69e8b48/tcr-11-07-2205-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/952eca568a03/tcr-11-07-2205-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/24bb9266ff7d/tcr-11-07-2205-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/aa62b732bc4b/tcr-11-07-2205-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/472822ad47bd/tcr-11-07-2205-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/69b4d935fa89/tcr-11-07-2205-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/3da311d0b78b/tcr-11-07-2205-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/ed3dcb8ca936/tcr-11-07-2205-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/31898e689fbf/tcr-11-07-2205-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/861fb69e8b48/tcr-11-07-2205-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/952eca568a03/tcr-11-07-2205-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/24bb9266ff7d/tcr-11-07-2205-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/aa62b732bc4b/tcr-11-07-2205-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/472822ad47bd/tcr-11-07-2205-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/69b4d935fa89/tcr-11-07-2205-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/3da311d0b78b/tcr-11-07-2205-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b90/9372201/ed3dcb8ca936/tcr-11-07-2205-f9.jpg

相似文献

1
GLIPR1 regulates the TIMP1-CD63-ITGB1-AKT signaling pathway in glioma cells and induces malignant transformation of astroglioma.GLIPR1调节胶质瘤细胞中的TIMP1-CD63-ITGB1-AKT信号通路，并诱导星形胶质瘤发生恶性转化。
Transl Cancer Res. 2022 Jul;11(7):2205-2216. doi: 10.21037/tcr-21-2413.
2
Timp1 interacts with beta-1 integrin and CD63 along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway independently of Akt phosphorylation.Timp1 在黑色素瘤发生过程中与β-1 整联蛋白和 CD63 相互作用，并通过激活 PI3-K 信号通路而不依赖 Akt 磷酸化来赋予抗失巢凋亡能力。
Mol Cancer. 2013 Mar 25;12:22. doi: 10.1186/1476-4598-12-22.
3
Integrin β1 regulates proliferation, apoptosis, and migration of trophoblasts through activation of phosphoinositide 3 kinase/protein kinase B signaling.整合素 β1 通过激活磷酸肌醇 3 激酶/蛋白激酶 B 信号通路调节滋养细胞的增殖、凋亡和迁移。
J Obstet Gynaecol Res. 2021 Jul;47(7):2406-2416. doi: 10.1111/jog.14782. Epub 2021 Apr 11.
4
TPX2-p53-GLIPR1 regulatory circuitry in cell proliferation, invasion, and tumor growth of bladder cancer.膀胱癌中 TPX2-p53-GLIPR1 调控回路在细胞增殖、侵袭和肿瘤生长中的作用。
J Cell Biochem. 2018 Feb;119(2):1791-1803. doi: 10.1002/jcb.26340. Epub 2017 Sep 11.
5
Glioma pathogenesis-related protein 1 exerts tumor suppressor activities through proapoptotic reactive oxygen species-c-Jun-NH2 kinase signaling.胶质瘤发病机制相关蛋白1通过促凋亡活性氧-c-Jun氨基末端激酶信号传导发挥肿瘤抑制作用。
Cancer Res. 2008 Jan 15;68(2):434-43. doi: 10.1158/0008-5472.CAN-07-2931.
6
GLIPR1 inhibits the proliferation and induces the differentiation of cancer-initiating cells by regulating miR-16 in osteosarcoma.GLIPR1通过调节骨肉瘤中的miR-16抑制癌症起始细胞的增殖并诱导其分化。
Oncol Rep. 2016 Sep;36(3):1585-91. doi: 10.3892/or.2016.4949. Epub 2016 Jul 19.
7
GLIPR1 modulates the response of cisplatin-resistant human lung cancer cells to cisplatin.GLIPR1调节顺铂耐药的人肺癌细胞对顺铂的反应。
PLoS One. 2017 Aug 3;12(8):e0182410. doi: 10.1371/journal.pone.0182410. eCollection 2017.
8
Pancreatic Premalignant Lesions Secrete Tissue Inhibitor of Metalloproteinases-1, Which Activates Hepatic Stellate Cells Via CD63 Signaling to Create a Premetastatic Niche in the Liver.胰腺前恶性病变分泌组织金属蛋白酶抑制剂-1，通过 CD63 信号激活肝星状细胞，在肝脏中形成一个前转移龛。
Gastroenterology. 2016 Nov;151(5):1011-1024.e7. doi: 10.1053/j.gastro.2016.07.043. Epub 2016 Aug 6.
9
Glioma pathogenesis-related protein 1 performs dual functions in tumor cells.胶质母细胞瘤发病相关蛋白 1 在肿瘤细胞中发挥双重功能。
Cancer Gene Ther. 2022 Mar;29(3-4):253-263. doi: 10.1038/s41417-021-00321-9. Epub 2021 Mar 19.
10
Microrchidia family CW‑type zinc finger 2 promotes the proliferation, invasion, migration and epithelial‑mesenchymal transition of glioma by regulating PTEN/PI3K/AKT signaling via binding to N‑myc downstream regulated gene 1 promoter.微线体家族 CW 型锌指蛋白 2 通过结合 N‑myc 下游调节基因 1 启动子调控 PTEN/PI3K/AKT 信号通路，促进胶质瘤的增殖、侵袭、迁移和上皮间质转化。
Int J Mol Med. 2022 Feb;49(2). doi: 10.3892/ijmm.2021.5071. Epub 2021 Dec 16.

引用本文的文献

1
CAP superfamily proteins in human: a new target for cancer therapy.人类 CAP 超家族蛋白：癌症治疗的新靶点。
Med Oncol. 2024 Nov 5;41(12):306. doi: 10.1007/s12032-024-02548-6.
2
Identification and validation of an ECM organization-related gene signature as a prognostic biomarker and therapeutic target for glioma patients.鉴定和验证一个与细胞外基质组织相关的基因标志物，作为胶质母细胞瘤患者的预后生物标志物和治疗靶点。
Genes Genomics. 2023 Sep;45(9):1211-1226. doi: 10.1007/s13258-023-01413-6. Epub 2023 Jun 10.

本文引用的文献

1
Prognostic Value of CD63 Expression in Solid Tumors: A Meta-analysis of the Literature.CD63 表达在实体瘤中的预后价值：文献的荟萃分析。
In Vivo. 2020 Sep-Oct;34(5):2209-2215. doi: 10.21873/invivo.12031.
2
THBS4 promotes HCC progression by regulating ITGB1 via FAK/PI3K/AKT pathway.THBS4 通过 FAK/PI3K/AKT 通路调控 ITGB1 促进 HCC 进展。
FASEB J. 2020 Aug;34(8):10668-10681. doi: 10.1096/fj.202000043R. Epub 2020 Jun 22.
3
The unicellular eukaryotic parasite Toxoplasma gondii hijacks the migration machinery of mononuclear phagocytes to promote its dissemination.
单细胞真核寄生虫刚地弓形虫劫持单核吞噬细胞的迁移机制来促进其传播。
Biol Cell. 2020 Sep;112(9):239-250. doi: 10.1111/boc.202000005. Epub 2020 May 19.
4
Comprehensive gene and pathway analysis of cervical cancer progression.宫颈癌进展的综合基因与通路分析
Oncol Lett. 2020 Apr;19(4):3316-3332. doi: 10.3892/ol.2020.11439. Epub 2020 Mar 3.
5
Establishment of Structure-Function Relationship of Tissue Inhibitor of Metalloproteinase-1 for Its Interaction with CD63: Implication for Cancer Therapy.基质金属蛋白酶组织抑制剂-1 结构与功能关系的建立与其与 CD63 的相互作用：对癌症治疗的启示。
Sci Rep. 2020 Feb 7;10(1):2099. doi: 10.1038/s41598-020-58964-x.
6
FRK suppresses human glioma growth by inhibiting ITGB1/FAK signaling.FRK 通过抑制 ITGB1/FAK 信号通路抑制人胶质瘤的生长。
Biochem Biophys Res Commun. 2019 Oct 1;517(4):588-595. doi: 10.1016/j.bbrc.2019.07.059. Epub 2019 Aug 5.
7
TIMP-1 promotes hypermigration of -infected primary dendritic cells via CD63-ITGB1-FAK signaling.TIMP-1 通过 CD63-ITGB1-FAK 信号促进感染的原代树突状细胞的过度迁移。
J Cell Sci. 2019 Feb 4;132(3):jcs225193. doi: 10.1242/jcs.225193.
8
CD31 regulates metastasis by inducing epithelial-mesenchymal transition in hepatocellular carcinoma via the ITGB1-FAK-Akt signaling pathway.CD31 通过 ITGB1-FAK-Akt 信号通路诱导肝癌发生上皮-间充质转化从而调控转移。
Cancer Lett. 2018 Aug 10;429:29-40. doi: 10.1016/j.canlet.2018.05.004. Epub 2018 May 8.
9
Co-expression of TIMP-1 and its cell surface binding partner CD63 in glioblastomas.TIMP-1 及其细胞表面结合伴侣 CD63 在脑胶质瘤中的共表达。
BMC Cancer. 2018 Mar 9;18(1):270. doi: 10.1186/s12885-018-4179-y.
10
TIMP1 promotes multi-walled carbon nanotube-induced lung fibrosis by stimulating fibroblast activation and proliferation.TIMP1通过刺激成纤维细胞活化和增殖促进多壁碳纳米管诱导的肺纤维化。
Nanotoxicology. 2017 Feb;11(1):41-51. doi: 10.1080/17435390.2016.1262919. Epub 2016 Dec 9.